Role of Faecalibacterium prausnitzii in Crohn's Disease: friend, foe, or does not really matter?
Role of Faecalibacterium prausnitzii in Crohn's Disease: friend, foe, or does not really matter?
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普氏粪杆菌在克罗恩病中的作用：朋友、敌人，还是并不重要？
DOI：
10.1097/mib.0000000000000079
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发表时间：
2014
影响因子：
4.9
通讯作者：
Gerasimidis K
中科院分区：
文献类型：
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作者：
Gerasimidis K
E18 | www。ibdjournal。我们认识到幽门螺杆菌是消化性溃疡和随后的胃癌发生的主要原因，并寻求根据观察到的证据来适应理论，而不是相反的立场。在文献中将细菌种类划分为“好的”和“坏的”有机体，这在生物学上是一种幼稚的观点，但在叙述上却很方便，它忽略了亚种或菌株特异性的特征。有两种物种需要谨慎对待，一种是大肠杆菌，它与许多疾病有关，包括在CD2中起关键作用，同时也长期被认为是一种成功的益生菌制剂3；另一种是脆弱拟杆菌，它在驱动免疫调节反应中发挥了明显的作用，同时也能够引发啮齿动物结肠炎。在这种情况下，至少应该考虑F. prausnitzii扮演一个比简单的“好人”更复杂的角色。我们不否认益生菌群失调是乳糜泻的一个特征，但迄今为止，在以前的研究中不能排除反向因果关系。Sokol等人先前的观察结果表明，在那些具有较高丰度的F. prausnitzii6的患者中，内窥镜复发率较低，这是有趣的，我们并不破坏支持丁酸盐在结肠健康中的抗炎特性和生物学作用的证据。然而，我们要强调的是，我们小组之前的研究表明，未接受治疗的儿童在诊断时粘膜F. prausnitzii增加，7并且先前的研究也表明，成人在EEN治疗期间出现临床反应的F. prausnitzii减少。8总的来说，这些挑战了目前的模式，即该物种的增加总是对乳糜泻患者有益。此外，大多数使用益生元和/或益生菌诱导或维持乳糜泻患者临床缓解的干预研究结果令人失望9，丁酸灌肠剂的使用仅限于溃疡性结肠炎患者10或结肠炎的动物研究。它们不一定反映人类疾病的发病机制。我们同意肠道菌群在肠道相关免疫系统的激活中发挥重要作用，我们认为EEN通过抑制某些肠道菌群及其代谢诱导临床缓解并实现粘膜愈合。通过这种方式，细菌衍生介质对乳糜泻患者有缺陷的肠道相关免疫系统的激活减弱。高通量测序和代谢组学技术现在可以更好地表征整个微生物组及其在EEN和CD进化过程中的变化。未来的研究应该尝试描述肠内肠炎期间的主要细菌变化及其在对抗结肠炎症中的机制作用，而不是那些仅仅由于肠内肠炎饲料中缺乏纤维或其他原因而改变的副现象。这将允许开发专门针对乳糜泻的新型营养疗法，补充或不补充丁酸盐产生成分，以及使用食品级细菌来促进或不促进共生物种的生长，并为其他临床情况下乳糜泻的发病机制和治疗反应提供有用的信息。
E18| www. ibdjournal. org our recognition of Helicobacter pylori as the leading cause of peptic ulceration and subsequent gastric carcinogenesis and seek to fit theories around observed evidence and not the opposite stance. The division of bacterial species within the literature into “good” and “bad” organisms is a biologically naive but narratively convenient position that ignores subspecies or strain-specific traits. Two species that would advocate caution with this approach are Escherichia coli, associated with many diseases including a key role in CD2 while also being long recognized as a successful probiotic agent, 3 and Bacteroides fragilis having a demonstrable role in driving an immunoregulatory response4 while also being capable of initiating rodent colitis. 5 In this context, a more complex role for F. prausnitzii than simply a “good guy” should at least be considered. We do not dispute that a dysbiotic microbiota is a characteristic of CD, but thus far reverse causality cannot be ruled out in previous studies. The previous observation from Sokol et al of a lower endoscopic relapse rate in those patients who had a higher abundance of F. prausnitzii6 is intriguing and we do not undermine the evidence that supports the anti-inflammatory properties and biological role of butyrate in colonic health. We would, however, highlight previous work among our group that demonstrates that treatment naive children have increased mucosal F. prausnitzii at diagnosis, 7 and previous studies have also demonstrated a reduction in F. prausnitzii in adults during EEN treatment who show a clinical response. 8 Collectively, these challenge the current paradigm that increases in this species are always beneficial in patients with CD. Additionally, the large majority of intervention studies using prebiotics and/or probiotics to induce or maintain clinical remission in people with CD have produced disappointing results, 9 and usage of butyrate enemas has been limited to patients with ulcerative colitis10 or in animal studies of colitis, 11 which do not necessarily reflect disease pathogenesis in humans. We do agree that gut microbiota plays an important role in the activation of the gut-associated immune system, and we suggest that EEN induces clinical remission and achieves mucosal healing by suppressing certain species of the gut microbiota and their metabolism. This way, activation of the defective gut-associated immune system in patients with CD by bacterially derived mediators is diminished. High-throughput sequencing and metabolomics techniques now offer improved characterization of the entire microbiome and its changes during EEN and during CD evolution. Future studies should try to delineate the primary bacterial changes during EEN and their mechanistic role in countering colonic inflammation compared with those that are epiphenomena, altered simply by the lack of fiber in the EEN feeds or other reasons. This will allow the development of novel nutritional therapies tailored specifically to CD, supplemented with or without butyrate producing ingredients, and with food-grade bacteria to promote or not the growth of symbiotic species and providing useful information for the pathogenesis and response to treatment of CD in other clinical situations.
影响因子：
4.9
作者：
Gerasimidis, Konstantinos;Bertz, Martin;Edwards, Christine A.
通讯作者：
Edwards, Christine A.