银屑病与大肠相关机制（调研手稿五）

LPS诱导野生型大鼠肝损伤发生时，肝脏中TNF-α浓度显著升高

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(7) Some experts believe that psoriasis is actually caused by intestinal permeability, specifically in the area between the duodenum and the jejunum.

Consequently, the body seeks to eliminate the toxins through the skin. In this model, psoriasis represents the body’s desperate attempt to cleanse itself.（一些专家认为银屑病实际上是由肠道通透性引起的，特别是在十二指肠和空肠之间。因此，身体试图通过皮肤排除毒素。在这个模型中，银屑病代表着身体拼命地试图净化自己。）

Wild-caught fish — Fish like salmon, mackerel, herring and sardines are excellent sources of vitamin D as well as omega-3 fatty acids, which are both key to improving psoriasis. Vitamin D is clinically proven to help fight psoriasis. (15) If you have psoriasis, fish should be the new leading protein in your life rather than meat and conventional dairy products. Studies have shown that eating fewer protein-rich foods, primarily meats and dairy products, may help ease psoriasis flare-ups.

Raw dairy — Raw milk is a much healthier choice than conventional milk. Rich in vitamin D and enzymes, raw dairy products can be therapeutic to psoriasis.

Herbs and spices — Herbs and spices are anti-inflammatory and contain antioxidants. Curcumin, the active ingredient in the spice known as turmeric, is known for its potent health properties. A 2012 scientific review specifically notes turmeric’s ability to alter TNF cytokine expression, which are known to play an essential role in the start and continuation of psoriatic lesions. This is probably why patients find turmeric helpful in minimizing psoriasis and psoriatic arthritis flare-ups. You can liberally add this spice to your food, keeping in mind that the FDA considers 1.5 to 3.0 grams of turmeric per day safe. (16)

野生鱼类——鲑鱼、鲭鱼、鲱鱼和沙丁鱼等鱼类是维生素D以及ω-3脂肪酸的极好来源，这两种脂肪酸都是改善银屑病的关键。临床证明维生素D有助于对抗牛皮癣。（15）如果你患有银屑病，鱼应该是你生活中新的主要蛋白质，而不是肉和传统的乳制品。研究表明，少吃富含蛋白质的食物，主要是肉类和乳制品，可能有助于缓解牛皮癣的发作。

生牛奶-生牛奶比传统牛奶更健康。生奶制品富含维生素D和酶，可以治疗牛皮癣。

草药和香料-草药和香料具有抗炎作用，并含有抗氧化剂。姜黄素是香料姜黄中的活性成分，以其强大的健康特性而闻名。2012年的一项科学评论特别指出，姜黄能够改变TNF细胞因子的表达，已知TNF细胞因子在银屑病病变的开始和持续中起着至关重要的作用。这可能就是为什么患者发现姜黄有助于减少银屑病和银屑病关节炎发作的原因。你可以在食物中大量添加这种香料，记住FDA认为每天1.5到3.0克姜黄是安全的。(16)

These are the top five supplements I recommend for internal treatment of psoriasis:

Hydrochloric acid (1–3 capsules per meal) — Helps with protein digestion and decrease psoriasis flare-ups.
Fish oil (1,000–2,000 grams daily) — Fish oil is anti-inflammatory and can aid in the healing of psoriasis.
Vitamin D3 (5,000 IU daily) — Low levels of vitamin D may be associated with psoriasis.
Milk thistle (250 milligrams three times daily) —Milk thistle helps promote liver detoxification and reduces cellular growth.
Probiotics (50 billion units daily) — Probiotics improve digestion by increasing good bacteria and crowding out bad bacteria. Digestive issues are linked to psoriasis.
Bonus Remedies:
Other home remedies for psoriasis that can reduce symptoms include cleansing, bone broth, vitamin B12 and digestive enzymes. Also, getting 20 minutes of sunshine a day can greatly improve vitamin D levels naturally and is very therapeutic to psoriasis.

Essential oils for psoriasis like tea tree, lavender, frankincense, myrrh and geranium essential oil can bring relief to inflamed skin and support the healing process.

Tea tree oil — When you use tea tree for your psoriasis, you prevent infection while also reducing inflammation and stimulating the immune system to support your skin health. Scientific research has confirmed the psoriasis-reducing effects of tea tree oil. (17)

Lavender oil — With calming and anti-inflammatory properties, it helps soothe the skin while also promoting new skin growth and healing.

Frankincense oil — With antiseptic, antibacterial, antioxidant and anti-inflammatory properties, frankincense can help provide relief for stubborn psoriasis patches.

Myrrh oil — Excellent at healing the chapped, flakey and cracked skin of psoriasis patches.

Geranium oil — Geranium is great at improving circulation and decreasing inflammation. It also helps relieve stress.

Coconut oil — It’s not an essential oil, but it’s a great choice for a base oil. You should always dilute essential oils in a base oil before applying them to problem areas. Coconut oil has anti-inflammatory, very gentle and moisturizing.

EO recipe idea: Mix three drops of lavender oil and three drop of frankincense oil with on teaspoon of coconut oil and rub onto affected area.

It’s also a great idea to use these essential oils in aromatherapy for psoriasis. You can diffuse these oils as a natural method of stress relief.

以下是我推荐用于银屑病内部治疗的五大补充剂：

盐酸（每餐1-3粒）-有助于蛋白质消化和减少牛皮癣发作。

鱼油（每天1000-2000克）-鱼油具有抗炎作用，有助于牛皮癣的愈合。

维生素D3（每天5000 IU）-低水平的维生素D可能与牛皮癣有关。

奶蓟（每天三次，每次250毫克）-奶蓟有助于促进肝脏解毒和减少细胞生长。

益生菌（每天500亿单位）-益生菌通过增加有益细菌和排挤有害细菌来改善消化。消化问题与牛皮癣有关。

奖金补救措施：

其他可以减轻银屑病症状的家庭疗法包括清洁、骨汤、维生素B12和消化酶。此外，每天阳光照射20分钟可以大大提高维生素D水平，对牛皮癣有很好的治疗作用。

治疗银屑病的精油，如茶树、薰衣草、乳香、没药和天竺葵精油，可以缓解发炎的皮肤，支持愈合过程。

茶树油-当你用茶树治疗牛皮癣时，你可以预防感染，同时减少炎症，刺激免疫系统以支持你的皮肤健康。科学研究已经证实茶树油有减轻银屑病的作用。(17)

薰衣草油-具有镇静和抗炎特性，有助于舒缓皮肤，同时促进新皮肤生长和愈合。

乳香油-具有防腐、抗菌、抗氧化和抗炎特性，乳香可以帮助缓解顽固性银屑病斑块。

没药油-对牛皮癣斑的皲裂、片状和破裂的皮肤有很好的治疗作用。

老鹳草油-老鹳草在改善循环和减少炎症方面有很大的作用。它也有助于缓解压力。

椰子油-它不是一种精油，但它是基础油的一个很好的选择。在将精油涂抹到有问题的部位之前，你应该在基础油中稀释精油。椰子油具有消炎、非常温和和保湿的作用。

EO配方理念：将三滴薰衣草油和三滴乳香油与一茶匙椰子油混合，擦在患处。

在银屑病的芳香疗法中使用这些精油也是一个好主意。你可以将这些油作为一种自然的减压方法来扩散。

Scalp Psoriasis vs. Seborrheic Dermatitis
Certain skin diseases look like psoriasis but actually fit another diagnosis. One example of this is seborrheic dermatitis, a red, itchy rash that appears most often (but not always) on the scalp.

Seborrheic dermatitis (or “seborrhea”) seems to have roots in stress, genetic factors, a particular yeast that lives on skin, certain diagnoses or medications and cold, dry weather. Newborns, men and people with oily skin are at the highest risk of this particular form of dermatitis.

Dandruff is caused by seborrhea. Infants with the condition are often referred to as having “cradle cap,” as well as given an improper diagnosis of diaper rash when the redness occurs around the groin.

Like psoriasis, seborrheic dermatitis most often clears and flares throughout the lifetime. If you have symptoms of these disorders, see a dermatologist for a confirmed diagnosis and treatment options. Since seborrhea is not an autoimmune disease, treatment looks different – although many of the same items and supplements on my psoriasis diet are similar for those with seborrhea.

头皮牛皮癣与脂溢性皮炎

某些皮肤病看起来像牛皮癣，但实际上符合另一种诊断。其中一个例子是脂溢性皮炎，一种红色、发痒的皮疹，最常（但并非总是）出现在头皮上。

脂溢性皮炎（或“皮脂溢”）似乎源于压力、遗传因素、皮肤上的一种特殊酵母、某些诊断或药物以及寒冷干燥的天气。新生儿、男性和油性皮肤的人患这种特殊形式皮炎的风险最高。

头皮屑是由皮脂溢引起的。患有这种疾病的婴儿通常被称为“摇篮帽”，当腹股沟周围出现红肿时，也会被错误地诊断为尿布疹。

像牛皮癣一样，脂溢性皮炎通常在一生中都会消失和发作。如果您有这些疾病的症状，请向皮肤科医生咨询确认的诊断和治疗方案。由于皮脂溢不是一种自身免疫性疾病，治疗方法看起来有所不同——尽管我的银屑病饮食中许多相同的项目和补充剂对于皮脂溢患者来说是相似的。

上述信息来自【2】

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2.4. Artificial Sweeteners
Food additives have facilitated the development of the modern food industry. Normally, food additives (e.g., artificial sweeteners, emulsifiers, preservatives) are added in food products with an approved safe amount. Nevertheless, gut microbiome toxicity was not taken into consideration when the related standards were determined. Many artificial sweeteners are considered safe because they are poorly metabolized by the human body [29]. However, the gut bacteria are actively involved in the biotransformation. For example, cyclamate, which is currently banned in the USA, can be metabolized by gut bacteria into cyclohexylamine, which is carcinogenic [63]. Artificial sweeteners stevioside and xylitol can also be metabolized by the gut bacteria [64,65]. Several studies have demonstrated that some artificial sweeteners and emulsifiers were able to induce gut microbiome toxicity with potential gut microbiota-related health consequences. For instance, in an elegantly conducted study by Suez and colleagues, consumption of saccharin induced both compositional and functional changes in mouse gut microbiome that might be involved in the development of glucose intolerance [66]. Another study reported similar results with increased inflammatory levels in addition to gut microbial perturbation induced by saccharin in mice [15]. Additionally, artificial sweeteners acesulfame potassium [61], sucralose [67], aspartame [68], and neotame [69] can also perturb bacterial metabolites in concert with health implications including obesity and inflammation. Moreover, another study found that two commonly used emulsifiers altered mouse gut microbial composition together with elevated inflammatory levels [70].

2.4. 人工甜味剂

食品添加剂促进了现代食品工业的发展。通常，食品添加剂（例如，人工甜味剂、乳化剂、防腐剂）以批准的安全量添加到食品中。然而，在确定相关标准时，并未考虑肠道微生物组毒性。许多人造甜味剂被认为是安全的，因为它们在人体内代谢不良[29]。然而，肠道细菌积极参与生物转化。例如，甜蜜素，目前在美国被禁止，可以被肠道细菌代谢成致癌的环己胺[63]。人工甜味剂甜菊糖苷和木糖醇也可以被肠道细菌代谢[64,65]。一些研究表明，一些人工甜味剂和乳化剂能够诱导肠道微生物群毒性，并可能导致肠道微生物群相关的健康后果。例如，在苏伊士及其同事精心进行的一项研究中，食用糖精会导致小鼠肠道微生物组的组成和功能变化，这可能与葡萄糖不耐受的发生有关[66]。另一项研究报告了类似的结果，除了糖精诱导的小鼠肠道微生物扰动外，炎症水平增加[15]。此外，人工甜味剂乙酰磺胺钾[61]、三氯蔗糖[67]、阿斯巴甜[68]和纽甜[69]也会干扰细菌代谢物，从而影响健康，包括肥胖和炎症。此外，另一项研究发现，两种常用乳化剂改变了小鼠肠道微生物组成，同时升高了炎症水平[70]。

The ratio of Firmicutes and Bacteroidetes as well as the abundance of Enterobacteriaceae in the gut can be readily changed by chemicals such as carbendazim [108] and aspartame [68]. Thus, such taxonomic characteristics can serve as biomarkers of gut microbiome toxicity associated with health outcomes such as inflammation and obesity. Moreover, distinctive changes in functional profiles such as key metabolites and metabolic pathways could serve as more relevant biomarkers because alterations in functional profiles directly influence the host. For example, arsenic exposure perturbed the gut microbial metabolite profiles, especially indole-containing metabolites, isoflavone metabolites, and bile acids [12]. Alterations in these functional metabolites could be a potential new mechanism of arsenic toxicity, and particularly, changes of these metabolites (e.g., bile acids and indole-containing compounds) can be used as biomarkers of arsenic-induced gut microbiome toxicity. Likewise, consumption of artificial sweeteners is associated with increased levels of pro-inflammatory metabolites and genes in the gut microbiome. This may be used as bioindicators of artificial sweeteners-induced gut microbiome toxicity that consequently leads to inflammation [15,67]. In addition, diazinon changed the bacterial pathways and metabolites involved in neurotransmitters in a gender-dependent manner, indicating that those bacteria-derived neurotransmitters can be biomarkers to probe gut microbiome toxicity arising from chemicals that have neurological toxicity [13]. The gender-dependent effect also indicates individual variation in biomarkers of gut microbiome toxicity resulting from gender differences in the gut microbiome.

肠道微生物组毒性的生物标记物可以是细菌种类、基因或代谢物，甚至是这些标记物的组合。暴露于某些化学物质后肠道微生物组的特征性变化可用于指示特定外源性物质的暴露或影响，这为环境健康监测提供了一种新的、潜在的侵入性较小的方法。更重要的是，如果化学毒性的潜在机制涉及肠道微生物组的扰动和特定的功能改变，那么这些改变也可以用作环境驱动健康状况的潜在生物标志物。

最近的研究记录了暴露于各种外源性物质后肠道微生物组的功能变化（表1）[12,13,14,15,47,51,52,61,62,66,67,68,69,70,76106107108109]。肠道微生物谱的持续变化可能是与特定化学暴露相关的肠道微生物组毒性的潜在生物标志物。概述了微生物组成的变化模式和轨迹，提供了肠道微生物组毒性的生物标志物草图。厚壁菌/拟杆菌比率被认为是与宿主肥胖相关的肠道微生物群能量收集能力的指标[100]。同样，肠杆菌科与肠道炎症有关[110]。多菌灵[108]和阿斯巴甜[68]等化学物质很容易改变厚壁菌和拟杆菌的比例以及肠道内肠杆菌科的丰度。因此，这种分类特征可以作为与炎症和肥胖等健康结果相关的肠道微生物组毒性的生物标志物。此外，关键代谢物和代谢途径等功能特征的显著变化可以作为更相关的生物标志物，因为功能特征的改变直接影响宿主。例如，砷暴露扰乱了肠道微生物代谢产物，尤其是含有吲哚的代谢产物、异黄酮代谢产物和胆汁酸[12]。这些功能代谢物的改变可能是砷毒性的潜在新机制，特别是这些代谢物（例如胆汁酸和含吲哚化合物）的变化可作为砷诱导的肠道微生物毒性的生物标记物。同样，食用人造甜味剂与肠道微生物群中促炎代谢物和基因水平的增加有关。这可以用作人工甜味剂诱导的肠道微生物组毒性的生物指示物，从而导致炎症[15,67]。此外，二嗪农以性别依赖的方式改变了与神经递质相关的细菌途径和代谢物，表明这些细菌源性神经递质可以作为生物标记物，用于探测由具有神经毒性的化学品引起的肠道微生物组毒性[13]。性别依赖性效应还表明肠道微生物组毒性生物标志物的个体差异是由肠道微生物组的性别差异引起的。

该文中有张表格，对比不同学术文献对于肠道菌群的变化。

A. muciniphila, a mucin-degrading bacterium commonly present in human and mouse gut microbiome, has many probiotic effects in gut barrier function, glucose homeostasis, and inflammation in humans and diverse animal models [115,116,117,118,119]. Several studies reported targeted gut microbiome modulation with increased A. muciniphila population via consumption of whole foods or food components. For example, consumption of several berry fruits including cranberries and raspberries promoted increased content and enhanced function of A. muciniphila in the gut microbiome in rodent studies. Specifically, cranberry extract improved insulin sensitivity and reduced weight gain in concert with a significant increase of A. muciniphila in diet-induced obese mice [120]. Likewise, black raspberries boosted A. muciniphila population in the gut microbiome together with profound changes in microbial functions and metabolites [121,122,123]. The polyphenols abundant in berry fruits could be a reason that A. muciniphila thrives. Feeding polyphenols from grapes to mice showed similar results with a drastic increase of A. muciniphila [124]. The gut microbiome offers a link between polyphenols and their diverse beneficial effects because polyphenols are poorly absorbed and metabolized by the human body [124]. Meanwhile, A. muciniphila uses mucin as carbon, nitrogen, and energy sources [125]. Goblet cells are the major producer of mucin in the intestinal epithelium [126]. It is reported that the number of goblet cells and the thickness of intestinal mucosa were increased in rats fed oligofructose [127]. Therefore, oligofructose may be an alternative factor for the increase of A. muciniphila in mice fed berries, which is supported by the study that administration of oligofructose did increase the A. muciniphila population in the gut microbiome of mice [128]. Of particular interest, metformin, medication to treat type 2 diabetes, also promotes A. muciniphila population in the gut microbiome, which is believed to contribute to its therapeutic effects [129,130]. Perturbation by environmental toxic chemicals and modulation by dietary components regarding the gut microbiome are fundamentally similar, except with different expected outcomes. Knowledge of how gut microbes react to xenobiotics and dietary components will address gaps in our understanding of both perturbation and modulation of the gut microbiome.

6. Conclusions
To summarize, exposure to xenobiotics such as antibiotics, heavy metals, and artificial sweeteners induces gut microbiome toxicity. Compositional alterations and functional changes occur along with this process in the gut microbiome, which can serve as potential biomarkers of gut microbiome toxicity. These chemical-induced perturbations lead to human diseases via several mechanisms including changes in the metabolite profiles, diversity loss, and altered energy metabolism (Figure 2).

粘杆菌是一种粘蛋白降解菌，通常存在于人类和小鼠肠道微生物群中，在人类和各种动物模型的肠道屏障功能、葡萄糖稳态和炎症中具有许多益生菌效应[1151161119]。几项研究报告了通过食用全食或食物成分对肠道微生物群进行靶向调节，从而增加嗜粘菌种群。例如，在啮齿类动物研究中，食用几种浆果，包括蔓越莓和覆盆子，可促进黏菌在肠道微生物群中的含量增加和功能增强。具体而言，蔓越莓提取物改善了胰岛素敏感性，减少了体重增加，与饮食诱导肥胖小鼠中嗜粘液链球菌的显著增加一致[120]。同样，黑覆盆子增加了肠道微生物群中的粘杆菌数量，同时微生物功能和代谢物也发生了深刻的变化[121122123]。浆果中富含的多酚可能是粘果天牛生长旺盛的原因。将葡萄中的多酚喂食给小鼠也显示出类似的结果，即粘杆菌数量急剧增加[124]。肠道微生物群提供了多酚与其多种有益作用之间的联系，因为多酚被人体吸收和代谢不良[124]。同时，粘杆菌将粘蛋白用作碳、氮和能源[125]。杯状细胞是肠上皮中粘蛋白的主要产生者[126]。据报道，喂食低聚果糖的大鼠的杯状细胞数量和肠粘膜厚度增加[127]。因此，低聚果糖可能是喂食浆果的小鼠体内嗜粘液链球菌数量增加的一个替代因素，这一点得到了低聚果糖确实增加了小鼠肠道微生物群中嗜粘液链球菌数量的研究的支持[128]。特别令人感兴趣的是，治疗2型糖尿病的药物二甲双胍也促进了肠道微生物群中的嗜粘液链球菌数量，这被认为有助于其治疗效果[129130]。环境有毒化学物质的干扰和饮食成分对肠道微生物组的调节基本相似，但预期结果不同。了解肠道微生物对外源性物质和饮食成分的反应将弥补我们对肠道微生物组的干扰和调节的理解上的差距。

6.结论

总而言之，暴露于抗生素、重金属和人工甜味剂等外源性物质会导致肠道微生物组毒性。肠道微生物组的成分改变和功能改变伴随着这一过程而发生，可作为肠道微生物组毒性的潜在生物标志物。这些化学诱导的扰动通过几种机制导致人类疾病，包括代谢物谱的变化、多样性丧失和能量代谢的改变（图2）

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提到了：

香豆素

滨蒿内酯的衍生物

本研究中应用ConA 及LPS 分别刺激产生T 细胞和B 细胞，进而研究药
物对这两种细胞的作用

上述信息来自【4】

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Due to its crucial role in human fitness, the gut microbiome is now considered as a new organ in the human body [7,8,9]

肠道微生物组现在被视为一个器官

上述信息来自【10】

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上述信息来自【10】

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Gut Microbiome
The gut microbiome plays important roles in both the maintenance of health and the pathogenesis of disease. Gut microbiome dysbiosis, resulting from alterations of composition and function of the gut microbiome and disruption of gut barrier function, exists in patients with CKD. Gut microbiome dysbiosis generates excessive amounts of uremic toxins. Most of them are derived from the unbalanced fermentation of nitrogen compounds in relation to nondigestible carbohydrates, such as p-cresyl sulfate and indoxyl sulfate in particular. The impaired intestinal barrier permits translocation of these toxins into the systemic circulation. These uremic toxins have been implicated in the progression of CKD, development of cardiovascular disease, and risk of death in CKD patients.134,135 Evidence suggests that the gut microbiome is altered in patients with CKD.136 Several factors contributing to gut microbiome dysbiosis in CKD include decreased consumption of dietary fiber, constipation, impaired protein assimilation, antibiotic use, and iron therapy.134

肠道微生物组

肠道微生物群在维持健康和疾病发病机制中起着重要作用。CKD患者存在由肠道微生物组的组成和功能改变以及肠道屏障功能破坏引起的肠道微生物组失调。肠道微生物群失调会产生过量的尿毒症毒素。其中大多数来源于与不可消化碳水化合物相关的氮化合物的不平衡发酵，例如对甲酚硫酸盐和吲哚硫酸盐。受损的肠道屏障允许这些毒素进入体循环。这些尿毒症毒素与CKD的进展、心血管疾病的发展和CKD患者的死亡风险有关。134135证据表明，CKD患者的肠道菌群发生了改变。136导致CKD肠道菌群失调的几个因素包括膳食纤维的消耗减少，便秘、蛋白质同化受损、抗生素使用和铁疗法。134

先天免疫反应与精神病性疾病

来自【9】

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Exotoxins: These are the macromolecules of protein origin, which are produced and later released to the medium by the microorganism. Depending on their mechanism of action, exotoxins are divided as follows:

Toxins Type I. These toxins modify the host’s cells without internalizing in the cells; for example, the superantigens produced by Staphylococcus aureus and Streptococcus pyogenes.

Toxins Type II. Within this group there are hemolysins and phospholipases; this group of toxins is characterized by pore formation and/or destroying the membranes of the host cells. With this virulence factor, the pathogen can invade the host cell; for example, aerolysin and GCAT protein produced by Aeromonas spp.

Toxins Type III. These toxins are known as A/B due to their binary structure. Fraction B has the function of binding to the receptor of the cell and fraction A is the unit that possesses enzymatic activity, which, depending on the toxin and its mechanism of action, will be the damage to the cell; for example, the Shiga toxin produced by Escherichia coli O157:H7, the Cholera toxin (Ctx) produced by Vibrio cholerae, and the Anthrax toxin produced by Bacillus anthracis [5, 6].

Exotoxins of Gram-negative enteropathogenic bacteria play an important role in the pathogenesis of diarrheal disease, causing hypersecretion of liquids without the destruction and death of intestinal mucosal cells. These toxins are generically referred to as enterotoxins that are different from cytotoxins [8]

外毒素：这些是蛋白质来源的大分子，由微生物产生并随后释放到培养基中。根据其作用机制，外毒素分为以下几种：

第一类毒素。这些毒素修饰宿主细胞而不在细胞内消化；例如，金黄色葡萄球菌和化脓性链球菌产生的超抗原。

第二类毒素。在这一组中有溶血素和磷脂酶；这组毒素的特点是形成孔隙和/或破坏宿主细胞膜。有了这种毒力因子，病原体可以侵入宿主细胞；例如，气单胞菌产生的溶气素和GCAT蛋白。

毒素类型III。由于其二元结构，这些毒素被称为A/B。组分B具有与细胞受体结合的功能，组分A是具有酶活性的单位，根据毒素及其作用机制，这将是对细胞的损伤；例如，大肠杆菌O157:H7产生的志贺毒素、霍乱弧菌产生的霍乱毒素（Ctx）和炭疽杆菌产生的炭疽毒素[5,6]。

革兰氏阴性肠致病菌的外毒素在腹泻病的发病机制中起着重要作用，可导致液体分泌过多而不会破坏和死亡肠粘膜细胞。这些毒素一般称为肠毒素，不同于细胞毒素[8]

来自【12】

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The Gut Balance Revolution（一本书）

But actually, 90% of your serotonin is made in your GI tract! (13)

Cutting-edge research by Caltech scientists show that we depend on probiotics living in the gut to produce the serotonin we need to feel happy, focused, and confident. (12)

（产生自信的血清素来自肠道）

Experts agree that a balance of 85% probiotics and 15% bad microbes like Candida is ideal. (15)

专家们一致认为85%的益生菌和15%的有害微生物（如念珠菌）的平衡是理想的。(15)

Are you surprised to discover your “healthy” yogurt may have MORE sugar than a Twinkie?

Unfortunately, yogurt is just one of the MANY sugar-loaded products at the grocery store that masquerade as health food.（停止酸奶）

开始推销Vive Biotics

Dr. David Perlmutter, a leading expert on digestive health, says this:
“Taking a probiotic can significantly reduce “leaky gut” symptoms, and this may have a significant downstream effect in reducing inflammation, the cornerstone of virtually any of the degenerative diseases you can think of.” (26)

Dr. Frank Lipman, noted wellness expert
and best-selling author, raves:
“What I love about quality probiotics, is their almost miraculous ability to transform sick people into healthy ones quickly, simply and effectively without drugs, negative side effects or – dare I say it – much extra effort. I generally advise my clients to take probiotics daily to support optimal health.” (27)

（

消化健康方面的领先专家大卫·帕尔穆特博士说：

“服用益生菌可以显著减少“肠道渗漏”症状，这可能在减少炎症方面具有显著的下游效应，而炎症几乎是你能想到的任何退行性疾病的基石。”

著名健康专家弗兰克·利普曼博士

和畅销书作者，瑞夫斯：

“我喜欢高质量的益生菌，因为它们几乎奇迹般地能够快速、简单、有效地将病人转变为健康人，而无需药物、负面副作用或（我敢说）额外的努力。我通常建议我的客户每天服用益生菌，以支持最佳健康。”（27）

我同意利普曼博士的观点，我们应该每天服用益生菌。

）

Dr. Glen Gibson, Professor of Food Microbiology at Reading University, and one of the world's leading experts on digestive health, states a quality probiotic must meet the following three criteria to be safe and effective:

CRITERIA #1
The probiotic must contain LIVE good bacteria and they must STAY ALIVE during production and storage.

CRITERIA #2
The probiotic needs to be able to survive in the intestine. A lot of the probiotics you see at the store don’t work because they can’t survive the harsh acidic environment of your digestive system.

CRITERIA #3
The probiotic must contain at least five unique strains of good bacteria. (15)

雷丁大学食品微生物学教授、世界领先的消化健康专家之一格伦·吉布森博士指出，优质益生菌必须满足以下三个安全有效的标准：

标准#1

益生菌必须含有活菌，并且在生产和储存期间必须保持活性。

标准#2

益生菌需要能够在肠道中存活。你在店里看到的很多益生菌都不起作用，因为它们无法在你消化系统的严酷酸性环境中生存。

标准#3

益生菌必须至少含有五种独特的优良细菌。(15)

Here Is Why Vive Biotics Really Works
For starters, no other supplement we've seen can match the powerful blend of 15 unique probiotic strains we've included in Vive Biotics.

We included the probiotic strains L. plantarum, P. acidilactici, and S. thermophilus to help eliminate gas, bloating, stomach cramps, and indigestion by reducing growth and penetration of bad microbes in your GI tract.

We included B. bifidum for its proven ability to support nutrient absorption, particularly B-vitamin absorption, so you can turn more of your food into energy, not fat. (30)

We included strains that ease indigestion, lactose intolerance, and other common food sensitivities; strains that boost your immunity; and strains that protect against antibiotic-induced diarrhea.

We even included one strain, L. salivarius, that can help reduce plaque-forming bacteria in the mouth while naturally freshening breath and soothing gum sensitivity! (31)

首先，我们所看到的任何其他补充剂都无法与我们在Vive Biotics中包含的15种独特益生菌菌株的强大混合相媲美。

我们包括益生菌株植物乳杆菌、乳酸双歧杆菌和嗜热链球菌，通过减少有害微生物在胃肠道的生长和渗透，帮助消除胃气、腹胀、胃痉挛和消化不良。

我们将双歧杆菌包括在内是因为它被证明具有支持营养吸收的能力，特别是B-维生素吸收，所以你可以将更多的食物转化为能量，而不是脂肪。(30)

我们包括缓解消化不良、乳糖不耐症和其他常见食物敏感性的菌株；增强免疫力的菌株；以及防止抗生素引起腹泻的菌株。

我们甚至包括了一个菌株，唾液乳酸杆菌，它可以帮助减少口腔中形成菌斑的细菌，同时自然地清新口气和舒缓牙龈敏感！(31)

Unfortunately, the health aisle at your local drug store is like a probiotics graveyard.

Most probiotics have a shelf life of 6 to 12 months.

The dirty little secret the big probiotics manufacturers don’t want you to know is that their products are often 12 to 24 months old by the time they arrive on store shelves. You could be forking over your money for a probiotic that’s dead on arrival!

不幸的是，你当地药店的健康通道就像一个益生菌墓地。

大多数益生菌的保质期为6至12个月。

大型益生菌制造商不想让你知道的一个肮脏的小秘密是，他们的产品在上架时通常已经使用了12到24个月。你可能会掏钱买一种到达时就死了的益生菌！

这还不是最糟糕的…

当你买了一些益生菌的时候，它们是活的，不会保持这种状态很长时间。

大多数补充剂中只有3%到6%的活性益生菌能在肠道中存活下来。

在它们对你有任何好处之前，它们中的大多数会被你的胃酸所破坏。

但在这里，生命生物又是不同的。

上述内容来自【19】

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Pyruvate metabolism
Once pyruvate is produced, primarily from carbohydrates but also from other substrates, the human gut microbiota has developed several fermentation strategies to further generate energy, which are depicted in Fig. 1. Pyruvate can either be catabolized into succinate, lactate, or acetyl-CoA. However, these intermediates do not reach high concentrations in typical fecal samples, as they can be further metabolized by cross-feeders, producing the short-chain fatty acids (SCFAs) acetate, propionate, and butyrate (Table 1) [33]. These fecal metabolites are the most abundant and well-studied microbial end-products, since their effects are physiologically important: for example, host intestinal epithelial cells (IECs) utilize them as a source of fuel [62]. Indeed, SCFAs contribute approximately 10% of the caloric content required by the human body for optimal functioning [63]. Butyrate is the most preferred source of energy in this respect; its consumption improves the integrity of IECs by promoting tight junctions, cell proliferation, and increasing mucin production by Goblet cells [63, 64]. Butyrate also exhibits anti-inflammatory effects, through stimulating both IECs and antigen presenting cells (APCs) to produce the cytokines TGF-β, IL-10, and IL-18, and inducing the differentiation of naïve T cells to T regulatory cells [65]. Acetate and propionate can also be consumed by IECs (though to a much lesser degree than butyrate) and have some anti-inflammatory effects [33, 63]. Both acetate and propionate can dampen pro-inflammatory cytokine production mediated by toll-like receptor (TLR) 4 stimulation, and propionate, similar to butyrate, can induce the differentiation of T cells to T regulatory cells [33, 34]. Excess SCFAs that are not metabolized by IECs are transported via the hepatic vein to the liver, where they can be incorporated as precursors into gluconeogenesis, lipogenesis, and cholesterologenesis [62]. Specifically, propionate is gluconeogenic, whereas acetate and butyrate are lipogenic. The ratio of propionate to acetate is thought to be particularly important, as propionate can inhibit the conversion of acetate to cholesterol and fat [62, 66]. Indeed, propionate administration alone can reduce intra-abdominal tissue accretion and intrahepatocellular lipid content in overweight adults [67]. The role(s) of SCFAs in glucose homeostasis is/are not yet fully elucidated, although preliminary work has additionally suggested a beneficial effect, since plasma insulin levels are inversely related to serum acetate concentrations [62, 68].

丙酮酸代谢

一旦丙酮酸主要由碳水化合物产生，但也由其他底物产生，人类肠道微生物群已开发出几种发酵策略以进一步产生能量，如图1所示。丙酮酸可以分解为琥珀酸、乳酸或乙酰辅酶A。然而，这些中间产物在典型粪便样本中的浓度不高，因为它们可以通过交叉喂食者进一步代谢，产生短链脂肪酸（SCFA）醋酸盐、丙酸盐和丁酸盐（表1）[33]。这些粪便代谢物是最丰富且研究最充分的微生物终产物，因为它们的作用在生理上很重要：例如，宿主肠上皮细胞（IEC）将其用作燃料来源[62]。事实上，SCFA贡献了人体最佳功能所需热量的10%左右[63]。在这方面，丁酸是最优选的能源；它的消耗通过促进紧密连接、细胞增殖和杯状细胞增加粘蛋白的产生来改善IEC的完整性[63,64]。丁酸盐还具有抗炎作用，通过刺激IECs和抗原呈递细胞（APC）产生细胞因子TGF-β、IL-10和IL-18，并诱导原始T细胞分化为T调节细胞[65]。乙酸盐和丙酸盐也可被IECs消耗（尽管程度远低于丁酸盐），并具有一定的抗炎作用[33,63]。醋酸盐和丙酸盐均可抑制由toll样受体（TLR）4刺激介导的促炎症细胞因子的产生，丙酸盐与丁酸盐类似，可诱导T细胞分化为T调节细胞[33,34]。未被IECs代谢的多余SCFA通过肝静脉运输到肝脏，在那里它们可以作为前体并入糖异生、脂肪生成和胆固醇生成[62]。具体来说，丙酸盐是糖异生的，而乙酸盐和丁酸盐是脂异生的。丙酸盐与乙酸盐的比例被认为特别重要，因为丙酸盐可以抑制乙酸盐转化为胆固醇和脂肪[62,66]。事实上，在超重成人中，单独服用丙酸盐可以减少腹腔内组织增生和肝细胞内脂质含量[67]。SCFA在葡萄糖稳态中的作用尚未完全阐明，尽管初步研究还表明了有益的作用，因为血浆胰岛素水平与血清醋酸盐浓度呈负相关[62,68]。

上述内容来自【16】

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Twenty-five gut-derived, protein-bound uremic toxins have been described to date. They can be divided into six primary categories: advanced glycation end-products, hippurates, indoles, phenols, polyamines, and other (Table 1). Protein-bound toxins pose a unique problem in patients suffering from end-stage renal disease (ESRD) as the most effective techniques for removing uremic toxins—dialysis and hemofiltration—are unsuccessful against these molecules. Because PBUTs are not free floating in circulation, only a small fraction of unbound solute is susceptible to the concentration and pressure gradients used to draw waste out of the blood[8]. No therapeutic or other techniques are available to reduce serum levels of gut-derived PBUTs. Therefore, patients have no options to combat uremic syndrome caused by PBUTs, and the subsequent progression from CKD into ESRD.

迄今为止，已有25种肠源性蛋白结合型尿毒症毒素被描述。它们可分为六大类：晚期糖基化终产物、马尿酸盐、吲哚、酚类、多胺和其他（表1）。蛋白结合毒素在患有终末期肾病（ESRD）的患者中是一个独特的问题，因为去除尿毒症毒素的最有效技术透析和血液滤过对这些分子不成功。由于PBUT在循环中不是自由漂浮的，因此只有一小部分未结合的溶质容易受到用于从血液中排出废物的浓度和压力梯度的影响[8]。目前尚无治疗或其他技术可用于降低肠源性PBUT的血清水平。因此，患者没有选择来对抗PBUTs引起的尿毒症综合征，以及随后从CKD进展到ESRD。

Gut-Derived PBUT Class	Toxin	Derivation	Pathological Mechanisms	Associated Comorbidities
AGEs	3-Deoxyglucosone Fructoselysine Glyoxal Methylglyoxal N(6)-Carboxymethyllysine Pentosidine	Diet	ECM crosslink formation Impaired endothelial progenitor cell function NF- kB/MAPK/JNK signaling RAGE signaling	Arterial stiffness Diabetic nephropathy Endothelial dysfunction Immune system dysregulation
Hippurates	Hippuric acid Hydroxyhippuric acid	Diet	Activation of mitochondrial fission Albumin binding Free radical production NF- kB signaling	Altered drug pharmacokinetics Endothelial dysfunction Renal tubule damage
Indoles	Indole-3-acetic acid Indoxyl glucuronide Indoxyl sulfate Kynurenine Kynurenic acid Melatonin Quinolinic acid	Microbial metabolism	AhR activation Excessive glutamate release Impaired mitochondrial OXPHOS NF- kB/MAPK signaling NMDA receptor activation Reduced PTH expression	Bone disease Cardiovascular disease Endothelial dysfunction Inflammation Muscle weakness/atrophy Neurotoxicity Oxidative stress
Phenols	Hydroquinone p-cresyl glucuronide p-cresyl sulfate Phenol Phenylacetic acid	Microbial metabolism	Apoptosis Chromosomal aberrations Inhibition of iNOS expression NADPH oxidase activation ROS production Stimulates Rho-associated protein kinase	All-cause mortality Cardiovascular disease Inflammation Oxidative stress Renal fibrosis Vascular remodeling
Polyamines	Putrescine Spermidine Spermine	Microbial metabolism/Diet	Inhibition of erythropoietin	Anemia
Other	CMPF Homocysteine	Diet	Albumin binding Altered hepatic metabolism CMPF radical adducts Competitive reabsorption by OAT Degradation of gut epithelial TJ VSMC proliferation	Altered drug pharmacokinetics Atherosclerosis Increased intestinal permeability Neurological abnormalities Renal tubule damage

上述内容来自【17】

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Table 1 Examples of foods, nutrients, and dietary patterns that influence human health linked to their effect on the gut microbiota
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High-intensity sweeteners are commonly used as sugar alternatives, being many times sweeter than sugar with minimal calories. Despite being “generally recognised as safe” by regulatory agencies, some animal studies have shown that these sugar substitutes may have negative effects on the gut microbiota.46 Sucralose, aspartame, and saccharin have been shown to disrupt the balance and diversity of gut microbiota.46 Rats given sucralose for 12 weeks had significantly higher proportions of Bacteroides, Clostridia, and total aerobic bacteria in their guts and a significantly higher faecal pH than those without sucralose.47 Mice given sucralose for six months had an increase in the expression in the gut of bacterial pro-inflammatory genes and disrupted faecal metabolites.48

Food additives, such as emulsifiers, which are ubiquitous in processed foods, have also been shown to affect the gut microbiota in animals.49 Mice fed relatively low concentrations of two commonly used emulsifiers—carboxymethylcellulose and polysorbate-80—showed reduced microbial diversity compared with mice not fed with emulsifiers. Bacteroidales and Verrucomicrobia were decreased and inflammation promoting Proteobacteria associated with mucus was enriched .49

Other areas of concern include the side effects of popular restrictive diets on gut health. These include some strict vegan diets, raw food or “clean eating” diets, gluten-free diets, and low FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) diets used to treat irritable bowel syndrome.

Vegans are viewed by some as healthier than omnivores. A study of 15 vegans and 16 ominvores found striking differences in serum metabolites generated by the gut microbes but very modest differences in gut bacterial communities.50 A controlled feeding experiment of 10 human omnivores randomised to receive either a high fat and low fibre diet or a low fat and high fibre for 10 days found very modest effects on gut microbiome composition and no difference in short chain fatty acid production. Together these data support a greater role for diet influencing the bacterial derived metabolome than just the short term bacterial community.50

Animal and in vitro studies indicate that gluten-free bread reduces the microbiota dysbiosis seen in people with gluten sensitivity or coeliac disease.5152 But most people who avoid gluten do not have coeliac disease or proved intolerance, and a recent large observational study showed an increased risk of heart disease in gluten avoiders, potentially because of the reduced consumption of whole grains.53 One study showed that 21 healthy people had substantially different gut microbiota profiles after four weeks on a gluten-free diet. Most people showed a lower abundance of several key beneficial microbe species.54

The low FODMAP diet has been shown in six randomised controlled trials to reduce symptoms of irritable bowel syndrome.5556 It is associated with a reduced proportion of Bifidobacterium in patients with irritable bowel syndrome, and responsiveness to this diet can be predicted by faecal bacterial profiles.57 Low FODMAP diets lead to profound changes in the microbiota and metabolome, the duration and clinical relevance of which are as yet unknown.5859

高强度甜味剂通常被用作糖的替代品，其甜度比热量最低的糖高出许多倍。尽管监管机构“普遍认为是安全的”，但一些动物研究表明，这些糖替代品可能对肠道微生物群产生负面影响。46三氯蔗糖、阿斯巴甜、，糖精已被证明会破坏肠道微生物群的平衡和多样性。46只给予三氯蔗糖12周的大鼠，其类杆菌、梭状芽孢杆菌、大肠杆菌和大肠杆菌的比例明显较高，与不含三氯蔗糖的小鼠相比，它们肠道中的需氧细菌总数和粪便pH值显著升高。47给予三氯蔗糖6个月的小鼠肠道中细菌促炎基因的表达增加，粪便代谢产物被破坏。48

加工食品中普遍存在的食品添加剂，如乳化剂，也已被证明会影响动物的肠道微生物群。49喂食相对较低浓度的两种常用乳化剂羧甲基纤维素和聚山梨酯-80的小鼠与未喂食乳化剂的小鼠相比，微生物多样性降低。类杆菌和疣状菌减少，与粘液相关的促炎蛋白细菌增多。49

其他值得关注的领域包括流行的限制性饮食对肠道健康的副作用。这些包括一些严格的素食饮食、生食或“清洁饮食”、无麸质饮食和用于治疗肠易激综合征的低FODMAP（可发酵低聚糖、双糖、单糖和多元醇）饮食。

一些人认为素食者比杂食者更健康。一项对15名素食主义者和16名不祥食者的研究发现，肠道微生物产生的血清代谢物存在显著差异，但肠道细菌群落的差异非常小。50一项对10名随机接受高脂肪低纤维饮食或低脂肪高纤维饮食10天的人类杂食动物进行的对照喂养实验发现，差异非常小对肠道微生物组成的影响，短链脂肪酸的产生没有差异。这些数据共同支持饮食对细菌代谢组的影响大于短期细菌群落。50

动物和体外研究表明，无麸质面包可减少麸质敏感或乳糜泻患者的微生物群失调。5152但大多数不吃麸质的人没有乳糜泻或证明不耐受，最近的一项大型观察研究表明，不吃麸质的人患心脏病的风险增加，可能是因为全谷物消费量的减少。53一项研究表明，21名健康人在无麸质饮食四周后，肠道微生物群的分布有很大不同。大多数人的几种关键有益微生物种类丰度较低。54

六项随机对照试验表明，低FODMAP饮食可减少肠易激综合征症状。5556它与肠易激综合征患者双歧杆菌比例降低有关，通过粪便细菌谱可以预测对这种饮食的反应。57低FODMAP饮食会导致微生物群和代谢组的深刻变化，其持续时间和临床相关性尚不清楚

上述内容来自【18】

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肠道结构

肠道结构	细分结构	作用
小肠	十二指肠空肠回肠	食物在小肠内受到胰液、胆汁和小肠液的化学性消化以及小肠的机械性消化,各种营养成分逐渐被分解为简单的可吸收的小分子物质在小肠内吸收.
大肠	盲肠(包括阑尾) 结肠(包括升结肠、结肠右曲、横结肠、结肠左曲、降结肠、乙状结肠)
直肠

上述内容来自【24】

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肠道菌群主要由厌氧菌、兼性厌氧菌和好氧菌组成。
胃、十二指肠、空肠细菌的种类及数量极少，至结肠细菌数
明显增加，浓度为109 ～ 12CFU/mL。目前已知的肠道微生物
群落可分为三大部分:

①与宿主共生的生理性细菌，为专性
厌氧菌，如双歧杆菌、类杆菌、优杆菌和消化球菌等，是肠道
的优势菌群，具有营养及免疫调节作用;

②与宿主共栖的条
件致病菌，以兼性需氧菌为主，为肠道非优势菌群，如肠球
菌、肠杆菌，肠道微生态平衡时无害，在特定的条件下对人
体有害;

③病原菌，大多为过路菌，长期定植的机会少，肠道
微生态平衡时无害，若数量超出正常水平，则可引起人体发
病，如变形杆菌、假单胞菌和韦氏梭菌等［6］

肠道正常微生物群与宿主的消化、营养、代谢、免疫等

密切相关，相当于人体后天获得的一个重要“器官”，对人
体生理活动具有重要的作用: ①营养作用: 肠道内一些正常
微生物，如双歧杆菌、乳杆菌等能合成多种蛋白质和维生素
供宿主利用。②防御作用: 正常微生物群定植在胃肠道黏
膜和胃肠道内容物中，形成胃肠道的动态微生态平衡，能阻
止外籍致病微生物的入侵和繁殖。③免疫调节作用: 胃肠
道的微生物能剌激宿主建立完备的免疫系统。正常微生物
不仅能刺激机体免疫器官的发育，而且对增强机体特异性
细胞和体液免疫是不可缺少的。

应激反应也称为狩猎式反应，在突然受到外界刺激
( 如创伤、手术、感染、饥饿等) 时，机体为保证心、脑组织的
血液供氧，在肠绒毛的血管袢处发生血流“短路”。动脉血
不经肠绒毛的毛细血管网直接进入肠绒毛静脉，引发肠黏
膜缺氧、坏死脱落、毛细血管网失去屏障，肠道正常细菌易
位入血［6， 14］，破坏肠道微生态平衡。长期累积形成体内慢
性感染源［14 － 15］，刺激机体产生多种细胞因子［16］，并导致天
然免疫功能失调［17］，形成了皮肤炎症( 表皮细胞角化过度
和角化不全等) 。
应激状态下，肠道正常菌群由原籍菌变为血液中的外
籍菌，初始细菌入血无明确的临床感染症状或体征。机体
免疫系统不能识别原籍菌易位所成为的外籍菌，在机体不
同环境和免疫功能作用下，外籍菌为适应生存而变异为部
分或完全缺壁的细菌，称细菌L 型［18 － 19］。有研究表明细
菌L 型是银屑病重要的致病菌。肠道细菌初始入血是细
菌型，刺激机体引起T、B 细胞的活跃趋势，各类细胞因子
产生，不断产生轻微的内源性感染，如初期的孤立红疹、瘙
痒等。机体正常免疫功能作用下，可以限制进入血流的
“外籍菌( 正常菌群) ”，不引起皮肤炎症性病变; 或红疹逐
渐消失，疾病转归。当肠道细菌不断入血，机体的内源性感
染损伤，免疫功能失调加重，逐渐转化为全身性疾病，即银
屑病所表现的慢性、炎症性、全身皮肤感染状态。

例如李佃贵认为脾失健运，产生“浊毒”，从调理脾胃、化浊
解毒治疗银屑病［22］; 刘朝霞采用健脾祛毒法治疗银屑
病［23 － 24］，均临床效果良好。

例如有临床采用龙骨、牡蛎、酸枣
仁、合欢皮等中药治疗观察银屑病，效果良好。

上述内容来自【25】

LEfSe 分析 [13] 通过线性判别分析（LDA）降维，在组与组之间寻
找具有统计学差异的生物标志物（Biomarker），进而评估差异物种影响
的大小，即得到LDA score（柱状图的长度）。图10 显示，LDA score>4
的物种，即组间丰度具有统计学差异的biomarker 共有13 个。在正常对
照组中，厚壁菌门（Firmicutes）及Fusicatenibacter 菌属显著增加；在银
屑病组中，Negativicutes、γ 蛋白杆菌（Gamma proteobacteria）、柔嫩梭
菌属(Faecalibacterium) 、unidentified_Enterobacteriaceae 、巨单胞菌属
（Megamonas）、大肠杆菌（Escherichia coli）、韦荣球菌科（Veillonellaceae）
等显著增加。

通过LEfSe 分析我们在两组粪便样本中共发现了13 种具有统计学
差异的物种。其中厚壁菌门以及fusicatenibacter 菌属在银屑病患者中显
著降低。2019 年任士萌等学者的一项关于非酒精性脂肪性肝病的研究发
现[16]，fusicatenibacter 与肿瘤坏死因子-α（TNF-α）的水平呈负相关，与
人体血清中高密度脂蛋白（HDL）的水平呈正相关。
TNF-α 是在银屑病发病中起重要作用的炎症因子之一 [17]。结合以上
结果我们推测，肠道中fusicatenibacter 丰度的降低可能是通过提高血清
中TNF-α 的水平在银屑病发病过程中起作用的。
目前大量流行病学调查发现银屑病患者心脑血管疾病的患病率高于
正常人[18]，且已知HDL 具有保护心血管的作用。因此考虑，该菌种在
肠道中水平的降低可能是通过降低血清中HDL 水平，而使银屑病患者
罹患心脑血管疾病的风险增加的。
在银屑病患者肠道中增加的菌种主要有：negativicutes、γ 蛋白杆菌
(gammaproteobacteria) 、柔嫩梭菌属(faecalibacterium) 、
unidentified_enterobacteriaceae、巨单胞菌属（egamonas）、大肠杆菌
（escherichia coli）、韦荣球菌科（veillonellaceae）等。

有研究显示韦荣球菌属可将葡萄糖和乳糖分解成短链脂肪酸。这些
短链脂肪酸不能合成粘蛋白，但会导致肠粘膜通透性增加，并促进肠道
炎症的形成[19]。银屑病与炎症性肠病都属于慢性炎症性疾病，早有研究
发现银屑病与慢性炎症性疾病有类似的肠道菌群结构[21]。2014 年英国学
者的一项研究发现，在炎症性肠病患者的肠道中韦荣球菌科
（Veillonellaceae）显著增加[20]。以上研究结果与我们的实验结果相一致

上述内容来自【26】

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提到了 omega3

单不饱和脂肪酸

地中海饮食

上述内容来自【27】

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（CRP）、TNF-和IL-6高于对照组。研究组采用of进行管理

一袋含有1 1010个菌落形成单位（CFU）活的婴儿双歧杆菌

每天35264次，持续6-8周（持续时间取决于疾病类型）。重要的

在这些患者中观察到血浆CRP、TNF-水平下降，但IL-6浓度没有下降

8周后的银屑病患者[26]。

Navarro-Lopez等人在。

涉及90名患者，他们服用三种益生菌菌株的混合物

长双歧杆菌CECT 7347、乳双歧杆菌CECT 8145和乳酸杆菌的比例为1:1:1

鼠李糖CECT 8361，每天一次，每个胶囊总共1 109 CFU，持续12周。A.

患者的PASI评分显著降低（理解为PASI-75降低）

66.7%的患者在12周后服用益生菌，41.9%的患者在12周后服用安慰剂。A.

6个月的随访显示，接受益生菌治疗的患者患糖尿病的风险较低

银屑病复发，因为给药细菌调节了它们的微生物群组成[27]。

SCFA是由未消化碳水化合物的厌氧发酵产生的

[28]. 它们是饱和脂肪族有机酸，由一到六个碳组成。

95%的SCFA为醋酸盐、丙酸盐、丁酸盐[30]。SCFA可以在两种情况下检测到

结肠和粪便以及肝脏、门静脉和外周血[31]。拟杆菌

该门主要生产醋酸盐和丙酸盐，厚壁菌门生产丁酸盐

[32]. SCFA具有多种功能：它们是结肠细胞的能量来源，

通过特异性G蛋白偶联受体参与脂质的调节

和葡萄糖代谢。此外，它们被作为底物或受体的器官吸收

信号分子[31]。丁酸具有抗炎作用，有助于维持上皮细胞

屏障，防止结肠炎。它还可以降低氧化应激并调节

Th17/Treg淋巴细胞之间的平衡。除厚壁菌门和拟杆菌门外，还有

Prevotella、Akkermansia、粪杆菌和瘤胃球菌，其中

在一些研究中也观察到，也产生SCFA[33]。尽管F/B标高较高

总体而言，微生物多样性的降低会影响到特定物种之间的平衡

SCFAs：乙酸的合成增加，丁酸的合成减少。自从

醋酸盐浓度与ghrelin水平和胰岛素抵抗呈正相关，

虽然丁酸浓度与炎症呈负相关[34,35]，但这种变化

在厚壁菌门和拟杆菌门中，影响SCFA水平的肠道中的大量可能是

银屑病和肥胖症的发病机制中的另一个常见途径，通常与之相关。

据我们所知，没有关于银屑病患者补充SCFAs的研究

目前尚未进行。SCFAs对银屑病的影响有待进一步研究

菌类	生产盐类
拟杆菌门	醋酸盐和丙酸盐
厚壁菌门	丁酸盐

.4. TMAO
The elevated F/B ratio was also observed by Cho et al. to increase the quantity of the
produced proatherogenic trimethylamine-N-oxide (TMAO), which may increase the risk
of cardiovascular diseases [40]. The dietary choline is metabolized by gut microbiota to
trimethylamine (TMA), which is a precursor of TMAO. L-carnitine, which is abundant e.g.,
in red meat, is also metabolized since its structure resembles choline. TMA is absorbed into
the blood, and then metabolized in the liver by hepatic flavin monooxygenase into TMAO,
which promotes reverse cholesterol transport, foam cell formation from macrophages,
atherosclerosis and plaque formation. Since the generation of TMAO is dependent on
gut microbiota, the significant reduction of plasma TMAO was observed in mice treated
with antibiotics [41]. Psoriasis, especially in its severe variant, is an independent factor
increasing cardiovascular risk. Psoriatic patients often suffer from hypertension and its
control is negatively correlated with the severity of the illness. Also, the prognosis after
myocardial infarct is worse in psoriatic patients than in the general population [42]. The
common alterations in gut microbiota, affecting the level of atherogenic TMAO and lipid
metabolism, may lie at the cause of such an observation. Nevertheless, further investigation
in order to confirm this hypothesis is still needed in the future.

5.4. TMAO

Cho等人也观察到F/B比率升高，以增加

产生促动脉粥样硬化的三甲胺-N-氧化物（TMAO），可能增加风险

心血管疾病的研究[40]。膳食胆碱由肠道微生物群代谢为

三甲胺（TMA），是TMAO的前体。左旋肉碱，含量丰富，例如。，

在红肉中，由于其结构类似于胆碱，因此也会被代谢。TMA被吸收到

然后通过肝脏黄素单加氧酶在肝脏代谢成TMAO，

促进胆固醇逆向转运，巨噬细胞形成泡沫细胞，

动脉粥样硬化和斑块形成。因为TMAO的产生取决于

肠道微生物群，治疗组小鼠血浆TMAO显著降低

使用抗生素[41]。银屑病，尤其是在其严重的变异，是一个独立的因素

增加心血管风险。银屑病患者常伴有高血压及其并发症

控制与疾病的严重程度呈负相关。另外，术后的预后

银屑病患者的心肌梗死比普通人群更严重[42]。这个

肠道微生物群的常见改变，影响致动脉粥样硬化TMAO和脂质水平

代谢，可能是这种观察的原因。然而，进一步调查

为了证实这一假设，未来仍需继续研究。

Vijayashankar和Raghunath于2012年在一家医院描述了一例脓疱性银屑病

47岁女性，成功接受产孢乳杆菌治疗

（未报告每剂CFU的具体数量）每天三次，并使用生物素b7

每天一次，每次10mg[75]

上面内容来自【28】

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Moreover, the study
revealed that medium-chain fatty acids (MCFAs,
hexanoate and heptanoate), which previously
showed antibacterial effects, were decreased in
both psoriasis groups [48].

此外，本研究

发现中链脂肪酸（MCFA，

己酸盐和庚酸盐），之前

显示出抗菌作用，在

两组银屑病患者[48]

Though short chain
fatty acids (SCFAs) were implicated to possess
anti-inflammatory effects on skin and produced
by Bacteroidetes, which are commonly
decreased in psoriasis, in this research, SCFAs
(acetate, butyrate, propionate) levels were
similar between groups.

Finally, Akkermansia
and Ruminococcus had positive correlation with
MCFAs (hexanoate, heptanoate), Akkermansia
alone was negatively corelated with fecal sIgA
and short chain fatty acids (acetate, butyrate)
and Coprobacillus had inverse correlation with
S100.

虽然短链

脂肪酸（SCFA）被认为具有

对皮肤和皮肤产生抗炎作用

由类杆菌引起，通常

在本研究中，银屑病患者SCFAs减少

（乙酸、丁酸、丙酸）水平为

组间相似。

最后，阿克曼西亚

而瘤胃球菌与感染呈正相关

阿克曼西亚MCFA（己酸、庚酸）

单独与粪便sIgA呈负相关

和短链脂肪酸（醋酸盐、丁酸盐）

粪杆菌与大肠杆菌呈负相关

S100

Additionally, none
of the discussed studies took into account antipsoriatic
therapies and diet (vegetarian, vegan,
gluten-free, lactose-free), which could possibly
influence immune status and microbiota
composition.

此外，没有

在所讨论的研究中，大多数都考虑了抗溃疡药

治疗和饮食（素食者、纯素者、，

不含麸质，不含乳糖），这可能

影响免疫状态和微生物群的组成。

The beneficial inhabitant of the human
intestine, F.prausnitzii (Firmucutes phylum),
produces butyrate (short chain fatty acid) that
provides energy for colonocytes, takes part in
protection from oxidative stress, possesses antiinflammatory
features and plays role in
regulation of T effector cells and regulatory T
cells (Tregs)[50-52].

人类的有益居民

肠，F.prausnitzii（厚壁菌门），

产生丁酸盐（短链脂肪酸），其

为结肠细胞提供能量，参与

保护免受氧化应激，具有抗炎作用

特点和作用

T效应细胞和调节性T淋巴细胞的调节

细胞（Tregs）[50-52]。

For example, Bifidobacteria
infantis (B.infantis), which was previously
reported to induce regulatory T cells in
peripheral blood of healthy participants, was
also shown to substantially decrease TNF-α, Creactive
protein levels and in a small extent IL-6
in 75% of psoriasis patients after 6-8 week of
daily probiotic intake[15, 56]. Notably, all these
pro-inflammatory biomarkers were increased in
psoriasis patients compared with the healthy
controls.

例如，双歧杆菌

婴儿（B.infantis），以前是

据报道，在小鼠体内诱导调节性T细胞

健康受试者的外周血

也显示出显著降低TNF-α，Creactive

蛋白质水平和少量IL-6

在治疗6-8周后，75%的银屑病患者

每日益生菌摄入量[15,56]。值得注意的是，所有这些

促炎性生物标志物在银屑病患者中增加（相比于健康人群而言）

fed them with Lactobacillus pentosus
(L.pentosus) GMNL-77 to look at symptoms
development and immune status differences.
Strains of L.pentosus has been implicated with
suppression of inflammatory mechanisms in
C.albicans infection in stomach, modulating
production of immunoglobulins A and M, IL-6,
IL-10, IFN-γ in intestines, reduction of microbial
lipopolysaccharide in guts and blood, decrease
of Firmicutes/Bacteroidetes ratio in intestines,
and possession of antibiotic properties [58-63].
The findings of Chen et al., 2017 [57] revealed
that mice given L.pentosus GMNL-77 had
significantly less psoriasis-like skin lesions and
decreased hyperproliferation of keratinocytes
compared with the imiquimod only treated
group. The probiotic-treated mice had reduced
expression levels of inflammatory biomarkers
such as TNF-α, IL-6, IL-23, IL-17A, IL-22 in skin.
Meanwhile, T cells’ (Th17 and Th22) number in
spleen and the organ’s size itself was reduced
as well. Though this study looked at skin and
spleen omitting gut microbiota composition and
intestinal immune status, its findings suggest
that probiotics can take role in alleviating
symptoms and inflammation in psoriasis and
provide new directions for usage of beneficial
bacteria in treatment of the psoriatic disease.

用戊糖乳杆菌喂养它们

（戊糖乳杆菌）GMNL-77检查症状

发育和免疫状态的差异。

戊糖乳杆菌的菌株与

抑制大鼠的炎症机制

胃白色念珠菌感染，调节

产生免疫球蛋白A和M，IL-6，

肠道中的IL-10、IFN-γ，减少微生物

肠道和血液中的脂多糖，减少

肠壁厚壁菌/类杆菌比率，

以及拥有抗生素特性[58-63]。

Chen等人2017年[57]的研究结果显示

给予戊糖乳杆菌GMNL-77的小鼠

明显减少牛皮癣样皮肤损伤和

角质形成细胞过度增殖减少

与仅治疗的咪喹莫特相比

组经益生菌处理的小鼠的死亡率降低

炎症生物标志物的表达水平

如皮肤中的TNF-α、IL-6、IL-23、IL-17A、IL-22。

同时，T细胞（Th17和Th22）数量增加

脾脏和器官本身的大小都缩小了

也虽然这项研究着眼于皮肤和皮肤

忽略脾脏的肠道微生物群组成和

研究结果表明，肠道免疫状态

益生菌可以起到缓解疾病的作用

银屑病和银屑病的症状和炎症

为有益的药物的使用提供新的指导

治疗银屑病的细菌

上述内容来自【29】

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成人AD患者粪便中双歧杆菌及乳酸杆菌的数量明显低于健康组，提示成人AD患者存在肠道菌群失调的情况。但少见成人AD患者的肠道菌群结构的研究。

上述内容来自【30】

######################################################################

The SCFAs propionate, acetate, and butyrate, coming from
the intestinal fermentation of dietary fiber, are decisive in the fact that the phenomenon of
bacterial translocation appears.

SCFA丙酸盐、乙酸盐和丁酸盐，来自肠道发酵的膳食纤维，在事实上是决定性的现象出现细菌移位。

It is known that Faecalibacterium
prausnitzii is a bacterium that induces the production of butyrate, but in the case of atopic
dermatitis it is hypothesized that non-producing subspecies are those that predominate in
the intestinal tract and that due to this fact they would not provide benefits to the general
situation of the patient [29]. Furthermore, Faecalibacterium genus showed the highest
presence and significant positive correlation with AD severity (SCORAD index) [30].
2.3. Probiotics in Atopic Dermatitis
Atopic dermatitis is the skin disease where the majority of studies carried out to
evaluate the effect of probiotics on the evolution of the disease are focused. In the study
published by our group, Navarro et al., a probiotic composed of Bifidobacterium lactis,
Bifidobacterium longum and Lactobacillus casei administered for 12 weeks was tested, observing
clinical and statistically significant differences at the end of the intervention period,
achieving a reduction in the SCORAD index of 80% in the probiotic group [31]. In gut
microbiota, genera Bacteroides, Ruminococcus, and Bifidobacterium significantly increased
their levels while Faecalibacterium decreased after probiotic consumption. [30]

众所周知，粪便杆菌

prausnitzii是一种细菌，可诱导丁酸盐的产生，但在过敏性疾病中

皮炎据推测，非生产性亚种是在皮肤中占优势的亚种

肠道，由于这一事实，它们不会给一般人带来好处

患者的情况[29]。此外，粪杆菌属表现最高

存在并与AD严重程度显著正相关（SCORAD指数）[30]。

2.3. 过敏性皮炎中的益生菌

特应性皮炎是一种皮肤病，大多数研究都是针对这种疾病进行的

重点评估益生菌对疾病演变的影响。在研究中

由我们的研究小组Navarro等人出版，一种由乳酸双歧杆菌组成的益生菌，

对服用12周的长双歧杆菌和干酪乳杆菌进行测试，观察

干预期结束时的临床和统计显著差异，

益生菌组的SCORAD指数降低80%[31]。内脏

微生物群、类杆菌属、瘤胃球菌属和双歧杆菌属显著增加

食用益生菌后，其粪便杆菌水平下降。[30]

文中提到了一张表格（关于益生菌治疗过敏性皮肤炎的）

Gerasimov et al. describe a significantly higher decrease in SCORAD in the intervention
group after 8 weeks of treatment with two specific strains of Lactobacillus acidophilus
and Bifidobacterium lactis together with prebiotics [35].

Gerasimov等人描述了干预中SCORAD的显著降低

组在治疗8周后使用两种特定菌株的嗜酸乳杆菌

乳酸双歧杆菌和益生元[35]。

The study carried out by van der Aa et al. It does not describe differences in SCORAD,
but it does confirm the presence of Bifidobacterium breve in stools after 12 weeks of ingestion,
a bacterium that was not detected in the stool of the patients at the beginning of the
study [36].
Shafiei et al. conducted an 8-week study with a treatment composed of seven probiotic
strains in which they did not obtain significant differences compared to placebo [37].
In the study developed by Farid et al., similar to the one described above, a mixture
of probiotics and prebiotics did obtain differences between groups in favor of probiotic
treatment in the evolution of SCORAD after 8 weeks of treatment [38].
Wu et al. detected a difference of more than 50% between groups in favor of probiotic
treatment in the SCORAD index, which represents a significant reduction after 10 weeks of
ingestion of Lactobacillus salivarius together with fructooligosaccharides [39].

（

van der Aa等人开展的研究没有描述SCORAD的差异，

但它确实证实了摄入12周后粪便中存在短双歧杆菌，

试验开始时，患者粪便中未检测到细菌

研究[36]。

Shafiei等人进行了一项为期8周的研究，其中包括七种益生菌

与安慰剂相比，它们没有获得显著差异的菌株[37]。

在Farid等人开发的研究中，与上述研究类似，一种混合物

益生菌和益生元组间的差异有利于益生菌

治疗8周后SCORAD演变中的治疗[38]。

Wu等人发现益生菌组之间的差异超过50%

治疗后，SCORAD指数显著下降，10周后显著下降

摄入唾液乳酸杆菌和低聚果糖[39]。

作为所有这些工作的总结，根据

参考文献将对特应性皮炎有更大的疗效，应包括

乳酸杆菌和双歧杆菌的菌株（几种菌株的组合）和微生物

2021年9月1513日第6次，共14次

治疗应至少延长至12周。在患有糖尿病的患者中，这种益处似乎更大

年龄超过三岁，且有家族病史者。

）

with plaque psoriasis, significant differences were observed in disease progression
when comparing the subgroup of cases which was administered a probiotic mixture of
12 weeks, compared to those taking placebo. The probiotic mixture used in this study was
composed of Bifidobacterium longum, Bifidobacterium lactis and Lactobacillus rhamnosus. At the
end of the study, patients from the probiotic group reached PASI75 by 66.7% versus 41.9%
by the placebo group [54]. Groeger et al. studied whether supplementation with a strain
of Bifidobacterium infantis for 6–8 weeks produced changes at the level of cytokines and
immunomarkers. In this work, it is concluded that the intake of the probiotic preparation
causes a significant reduction in the levels of C-reactive protein and TNF- when comparing
the data with those observed in the placebo group [55]. Finally, a third publication by
Vijayshankar et al. which describes the case of a patient with pustular psoriasis to which
the probiotic Lactobacillus sporogenes together with 10 mg of biotin was administered, in
15 days, a great improvement was observed in the patient, and almost complete bleaching
was reached by 4 weeks and remained free of lesions after 6 months of treatment [56].

斑块型银屑病在疾病进展方面存在显著差异

当比较服用益生菌混合物的亚组病例时

12周，与服用安慰剂的患者相比。本研究中使用的益生菌混合物为

由长双歧杆菌、乳双歧杆菌和鼠李糖乳杆菌组成。在

研究结束时，来自益生菌组的患者达到PASI75的比例分别为66.7%和41.9%

安慰剂组[54]。Groeger等人研究了是否添加菌株

婴儿双歧杆菌治疗6-8周后，细胞因子水平发生变化，并且

免疫标记物。在这项工作中，可以得出以下结论：益生菌制剂的摄入量

导致C-反应蛋白和TNF-水平显著降低

这些数据与安慰剂组中观察到的数据一致[55]。最后，由

Vijayshankar等人描述了一例脓疱性银屑病患者的情况

益生菌产孢乳酸杆菌与10 mg生物素一起服用

15天后，患者病情有了很大改善，几乎完全脱色

在4周时达到，并在治疗6个月后保持无病变[56]。

As a conclusion of the data described on the intestinal microbiota in psoriasis and
the little experience with clinical studies using probiotics, we can affirm that the data is
very encouraging regarding the adjunctive treatment with probiotics of this disease. The
results of our working group are the most conclusive [54], but we will have to wait for
more studies with the same probiotic mixture or new preparations that corroborate these
first results (Table 3).
Table 3. Probiotics and psoriasis.
Author Time of Treatment Probiotic Results
Navarro-López et al.
[54] 12 weeks
Bifidobacterium longum,
Bifidobacterium lactis and
Lactobacillus rhamnosus
Reduction in PASI: Patients with PASI reduction
up to 75% (PR: 66.7% vs. PL: 41.9%; p < 0.05)
Follow-up: Lower risk of relapse in PR
Groeger et al. [55] 6–8 weeks Bifidobacterium infantis
Significant reduction in the levels of C-reactive
protein and TNF- in PR
Vijayshankar et al. [56] 4 weeks Lactobacillus sporogenes +
biotin Case report

作为关于银屑病患者肠道微生物群和

虽然使用益生菌进行临床研究的经验很少，但我们可以肯定数据是正确的

对于这种疾病的益生菌辅助治疗非常令人鼓舞。这个

我们工作组的结果是最具决定性的[54]，但我们将不得不等待

更多关于相同益生菌混合物或新制剂的研究证实了这些结论

初步结果（表3）。

表3。益生菌和牛皮癣。

作者治疗益生菌结果的时间

纳瓦罗-洛佩斯等人。

[54]12周

长双歧杆菌，

乳双歧杆菌

鼠李糖乳杆菌

PASI降低：PASI降低的患者

高达75%（PR:66.7%，PL:41.9%；p<0.05）

随访：降低PR复发风险

Groeger等人[55]6-8周婴儿双歧杆菌

C-反应蛋白水平显著降低

PR中的蛋白质和TNF-

Vijayshankar等人[56]4周乳酸杆菌产孢菌+

生物素病例报告

4.1. Skin Microbiota in Acne
As previously described, the main dominant bacterial phyla on the skin are: Actinobacteria,
Proteobacteria, Bacteroidetes, and Firmicutes. More than 60% of the species
belong to the genera Staphylococcus (Firmicutes), Corynebacterium and Propionibacterium
(Actinobacteria), which vary greatly in their quantity depending on the characteristics
of the body region. In areas of oily skin (such as the back, scalp, and face) the lipophilic
species of Propionibacterium (including Cutibacterium) predominate. Moist regions (such
as the armpits, the groin area, or the soles of the hands and feet) are rich in Staphylococcus
and Corynebacterium species. Areas of dry skin (such as the forearm) have the most diverse
microbial community, with a mixture of all four phylum.
In the pilosebaceous gland, Cutibacterium acnes is the principal occupant, it represents
up to 90% of the microbiota in the body areas of oily skin. Its role in the pathophysiology
of acne has been the subject of study for the last century. However, there is currently no
consensus on its involvement in the development of the disease [63]. Other species, such
as Staphylococcus epidermidis, have been found in more abundant quantities in patients with
acne and in patients with active lesions. The participation of Malassezia species in acne
has also been documented, by observing cases of folliculitis associated with their presence.
Thus, some theories suggest that acne could be due more to a microbial interaction than to
the mere presence of a specific species [63].

4.1. 痤疮中的皮肤微生物群

如前所述，皮肤上主要的优势细菌门是：放线菌，

变形菌、拟杆菌和厚壁菌。超过60%的物种

属于葡萄球菌属、棒状杆菌属和丙酸杆菌属

（放线菌属），其数量因特征而有很大差异

身体部位的运动。在油性皮肤区域（如背部、头皮和面部），亲脂性皮肤

丙酸杆菌（包括角质杆菌）的种类占优势。潮湿地区（例如

腋窝、腹股沟或手足底）富含葡萄球菌

以及棒状杆菌。干燥皮肤的部位（如前臂）最为多样

微生物群落，由所有四门组成。

在毛皮脂腺中，痤疮表皮菌是主要的宿主，它代表

高达90%的微生物群分布在油性皮肤的身体部位。它在病理生理学中的作用

痤疮的治疗在上个世纪一直是研究的主题。然而，目前还没有

关于其参与疾病发展的共识[63]。其他物种，如

作为表皮葡萄球菌，已在患者中发现数量更为丰富的表皮葡萄球菌

痤疮和活动性病变患者。马拉色菌在痤疮发病中的作用

通过观察与其存在相关的毛囊炎病例，也有记录。

因此，一些理论认为，痤疮可能更多地是由于微生物的相互作用，而不是由细菌引起的

仅仅是某一特定物种的存在[63]。

In 2013 the team of Jung et al. used a probiotic mixture of Lactobacillus acidophilus,
Lactobacillus delbrueckii bulgaricus and Bifidobacterium bifidum in 45 adults with acne. There
was a 67% reduction in the lesion count at 12 weeks of treatment, and an 82% reduction
when combined with minocycline [70].
Kim et al. showed a decrease of 33.2% in the total count of lesions and 50% in
the content of fat at 12 weeks of treatment with Lactobacillus bulgaricus and Streptococcus
thermophiles [71].
In 2016, Fabbrocini et al. administered a Lactobacillus rhamnosus strain to a group of 20
individuals with acne for 12 weeks, obtaining a moderate improvement in patients when
compared with the placebo group [72].
In conclusion, in the case of acne and likewise with atopic dermatitis and psoriasis,
there is data supporting the role of the microbiota in origin and as a result, it is plausible to
think that the use of probiotics as adjunctive therapy, will play a relevant role in the future
treatment, evolution and prognosis of this disease (Table 4).

（2013年，Jung等人的团队使用了嗜酸乳杆菌的益生菌混合物，

45例成人痤疮患者的德氏乳杆菌和双歧杆菌。那里

治疗12周时，病变数量减少67%，减少82%

当与二甲胺四环素结合时[70]。

Kim等人的研究显示，病变总数减少了33.2%，而正常情况下减少了50%

保加利亚乳杆菌和链球菌治疗12周后的脂肪含量

嗜热菌[71]。

2016年，Fabbrocini等人将鼠李糖乳杆菌菌株注射给20名受试者

痤疮患者12周后，患者在

与安慰剂组相比[72]。

总之，对于痤疮和特应性皮炎和银屑病，

有数据支持微生物群在起源中的作用，因此，有可能

认为使用益生菌作为辅助治疗，将在未来发挥相关作用

本病的治疗、演变和预后（表4）。）

上述内容来自【31】

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The standard American diet is one that is high in linoleic
acid, mostly found in vegetable oils, nuts, seeds, and animal products.（美国的标准是高亚油酸食物）

In a later study involving 30 children with infantile seborrhoeic dermatitis, results demonstrated that those affected
with seborrhoeic dermatitis had elevations in serum essential fatty acids (P < 0.01) and decreased linoleic acid
(P < 0.001) compared to healthy controls, suggesting that
alterations in fatty acids may play a role in the development of seborrhoeic dermatitis.48 The incongruence
between these studies warrants further research into the
impact that fatty acids have on the development of seborrhoeic dermatitis.
Probiotics are live bacteria and yeast that interact beneficially with the digestive system. Kombucha, a fermented
tea, contains probiotics that may have positive therapeutic
implications for resolution of seborrhoeic dermatitis. Mahmoudi and colleagues examined the effect that kombucha
tea ethyl acetate fraction had against Malassezia species
isolated from 19 patients with seborrhoeic dermatitis.

在随后的一项涉及30名婴儿脂溢性皮炎患儿的研究中，结果表明，这些患者

脂溢性皮炎患者血清必需脂肪酸升高（P<0.01），亚油酸降低

（P<0.001）与健康对照组相比，表明

脂肪酸的改变可能在脂溢性皮炎的发生中起作用。48不协调

在这些研究之间，需要进一步研究

脂肪酸对脂溢性皮炎发展的影响。

益生菌是活的细菌和酵母菌，与消化系统有益地相互作用。发酵的康普茶（个人判断：基本属于瞎扯淡）

茶，含有益生菌，可能有积极的治疗作用

解决脂溢性皮炎的意义。Mahmoudi及其同事研究了康普茶的作用

茶乙酸乙酯组分对马拉色菌有抑制作用

分离自19例脂溢性皮炎患者。

具体食物

具体食物(中文)

促发炎饮食

Diets with high mean glycemic index11–13 • High intake of dairy products and casein15,17–19 • Whey protein21,22 • Foods high in leucine (dairy and red meat)13

• Diets with high mean glycemic index24,33 • High intake of dairy products24,33 • All bakery products (e.g., pizza, bread, cakes, etc.), vinegar, black tea, soy sauces, beer, wine, fermented cheese, mushrooms32

Hot beverages, spicy foods, caffeine, vanilla, cinnamon, niacin- (i.e., turkey, peanut, tuna, liver, chicken breast) and formalin-containing foods (i.e., crustacean, wet noodle, tofu, dried shitake mushroom), alcohol

平均血糖指数高11-13的饮食•乳制品和酪蛋白15,17-19的高摄入量•乳清蛋白21,22•亮氨酸（乳制品和红肉）高的食物13

•平均血糖指数高的饮食24,33•大量摄入乳制品24,33•所有烘焙产品（如比萨饼、面包、蛋糕等）、醋、红茶、酱油、啤酒、葡萄酒、发酵奶酪、蘑菇32

热饮料、辛辣食品、咖啡因、香草、肉桂、烟酸（即火鸡、花生、金枪鱼、肝脏、鸡胸肉）和含有福尔马林的食品（即甲壳类动物、湿面条、豆腐、干香菇）、酒精

推荐饮食

• Reduce foods with high mean glycemic index11–13 • Reduce intake of dairy products and casein15,17–19 • Discontinue use of whey protein21,22 • Reduce foods high in leucine (dairy and red meat)13

• Daily 90 mg zinc gluconate29–31 • Vegetables and fresh fruit, cereals that do not contain yeast (e.g., rice or corn cakes made with puffed cereals), white meats, eggs, vegetables, green tea, coffee32 • Discontinuation of diets with high Saccharomyces cerevisiae (beer, wine, bread, and other bakery products)3

Following rosacea-promoting diets, patients may use 0.8 mg SC naloxone hydrochloride to reduce the side effects44

Biotin supplements (preliminary).46 • Linoleic acid diet (preliminary).48 • Kombucha tea ethyl acetate, 80 mg/mL (in vivo studies needed)4

减少平均血糖指数高的食物11–13•减少乳制品和酪蛋白的摄入15,17–19•停止使用乳清蛋白21,22•减少亮氨酸含量高的食物（乳制品和红肉）13

•每日90毫克葡萄糖酸锌29–31•蔬菜和新鲜水果、不含酵母的谷物（例如，用膨化谷物制成的米糕或玉米饼）、白肉、鸡蛋、蔬菜、绿茶、咖啡32•停止高酿酒酵母饮食（啤酒、葡萄酒、面包和其他烘焙产品）3

在促进酒渣鼻饮食后，患者可使用0.8 mg SC纳洛酮盐酸盐以减少副作用44

生物素补充剂（初步）。46•亚油酸饮食（初步）。48•康普茶乙酸乙酯，80 mg/mL（需要体内研究）

上述内容来自【32】

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Concomitant administration of piperine 20 mg/kg increased
the serum concentration of curcumin for a short period
of 1 —2 h post drug. Time to maximum was significantly increased
(P < 0.02) while elimination half life and clearance significantly
decreased (P < 0.02), and the bioavailability was increased
by 154%. On the other hand in humans after a dose of
2 g curcumin alone, serum levels were either undetectable or
very low. Concomitant administration of piperine 20mg produced
much higher concentrations from 0.25 to 1 h post drug
(P < 0.01 at 0.25 and 0.5 h; P < 0.001 at 1 h), the increase in
bioavailability was 2000%. The study shows that in the dosages
used, piperine enhances the serum concentration, extent of absorption
and bioavailability of curcumin in both rats and humans
with no adverse effects.(姜黄素+胡椒碱)

上述内容来自【33】

########################################################################

Reference:

【1】肿瘤坏死因子在不同类型肝损伤中弄过的作用及机制研究（没看完）

【2】Psoriasis Diet and Natural Treatment Options - Dr. Axe

【3】Psoriasis Diet and Natural Treatment Options - Dr. Axe

【4】ADMC的药理活性及作用机制研究

【5】Gut Microbiome Toxicity: Connecting the Environment and Gut Microbiome-Associated Diseases(完成)

【6】Toxins | Free Full-Text | From the Gut to the Brain: Journey and Pathophysiological Effects of the Food-Associated Trichothecene Mycotoxin Deoxynivalenol | HTML(没有重要内容)

【7】Multifaceted Interactions of Bacterial Toxins With the Gastrointestinal Mucosa（打不开）

【8】Toxins Relevant to Gastrointestinal Disorders | SpringerLink(没有重要内容)

【9】Gut Microbiome - an overview | ScienceDirect Topics(没有重要内容)

【10】Bacterial Toxins Made in the Gut :: ChemViews Magazine :: ChemistryViews(没有重要内容)

【11】Frontiers | Mycotoxin: Its Impact on Gut Health and Microbiota | Cellular and Infection Microbiology（没有重要内容）

【12】Bacterial AB5 toxins inhibit the growth of gut bacteria by targeting ganglioside-like glycoconjugates | Nature Communications（没有重要内容）

【13】Food Poisoning Caused by Bacteria (Food Toxins) | IntechOpen（没有重要内容）

【14】"Leaky gut syndrome" - NHS（没有重要内容）

【15】Beta toxin is essential for the intestinal virulence of Clostridium perfringens type C disease isolate CN3685 in a rabbit ileal loop model - Sayeed - 2008 - Molecular Microbiology - Wiley Online Library（没有重要内容）

【16】Macronutrient metabolism by the human gut microbiome: major fermentation by-products and their impact on host health | Microbiome | Full Text（没有重要内容）

【17】Gut-Derived Protein-Bound Uremic Toxins | Encyclopedia（阅读完毕）

【18】Role of the gut microbiota in nutrition and health | The BMJ（阅读完毕）

【19】Do You Have These Symptoms?（阅读完毕）

【20】Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli()阅读完毕【20】Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli()

【21】LeakyGutFix – LeakyGutFix.com【22】Clostridioides difficile infection in adults: Clinical manifestations and diagnosis（阅读完毕）

【23】Gut Microbiome-Derived Uremic Toxin Levels in Hemodialysis Patients on Different Phosphate Binder Therapies - FullText - Blood Purification - Karger Publishers(阅读完毕)

【24】人体肠子的构造图_39问医生_39健康网

【25】银屑病与肠道菌群微生态调节机制探析 - 百度学术

【26】银屑病患者与健康人肠道菌群的比较研究 - 豆丁网

【27】Gut microbiota and nutrient interactions with skin in psoriasis: A
comprehensive review of animal and human studies

【28】Psoriasis and Gut Microbiome—Current State of Art

【29】(PDF) Elucidating Role of Bacteria in Psoriatic Disease: From Skin and Gut Perspectives

【30】免疫相关性皮肤病与胃肠道微生态

【31】Probiotics in the Therapeutic Arsenal of Dermatologists

【32】The role of nutrition in inflammatory pilosebaceous disorders: Implication of the skin-gut axis

【33】Influence of Piperine on the Pharmacokinetics of Curcumin in Animals and Human Volunteers

另外注意下ConA、肽聚糖这种毒素

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