Commensal bacteria, traditional and opportunistic pathogens, dysbiosis and bacterial killing in inflammatory bowel diseases.
Commensal bacteria, traditional and opportunistic pathogens, dysbiosis and bacterial killing in inflammatory bowel diseases.
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DOI：
10.1097/qco.0b013e32832a8a5d
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发表时间：
2009-06
影响因子：
3.9
通讯作者：
Sartor RB
中科院分区：
文献类型：
--
作者：
Packey CD;Sartor RB
作者提出了过去两年发表的证据，证明共生细菌和病原体在炎症性肠病(IBD)的发病机制中所起的作用。啮齿动物模型最终表明，在慢性、免疫介导的实验性结肠炎中存在共生肠道细菌，在克罗恩病患者的一部分患者中发现了遗传决定的先天性免疫细胞杀死细菌的缺陷。没有证据表明包括副结核分枝杆菌在内的单一病原体会引起克罗恩病或溃疡性结肠炎。然而，粘附性/侵袭性大肠埃希菌(AIEC)与回肠克罗恩病有关，其毒力机制和遗传学尚未阐明。对IBD患者微生物群的分子特征表明，共生细菌的生物多样性减少，最显著的是类杆菌门和Firmicuts，包括与临床相关的普鲁斯尼茨杆菌，而大肠杆菌浓度增加。VSL#3是一种在小型临床试验中被证明在某些临床情况下有效的益生菌制剂。进一步描述IBD患者中改变的微生物区系，并将生物失调与免疫调节、固有微生物杀伤和屏障功能方面的宿主遗传变化联系起来是至关重要的，以便能够针对特定的患者亚群量身定做增加有益共生体及其代谢产物(益生菌和益生菌给药)和减少有害物种(如AIEC)的个体化治疗。
The authors present evidence published during the past two years of the roles of commensal and pathogenic bacteria in the pathogenesis of the inflammatory bowel diseases (IBD). Rodent models conclusively implicate commensal enteric bacteria in chronic, immune-mediated, experimental colitis, and genetically determined defects in bacterial killing by innate immune cells are found in a subset of Crohn’s disease patients. There is no evidence that a single pathogen, including Mycobacterium avium subspecies paratuberculosis, causes Crohn’s disease or ulcerative colitis. However, adherent/invasive E. coli (AIEC) are associated with ileal Crohn’s disease, with the mechanisms and genetics of AIEC virulence being elucidated. Molecular characterization of the microbiota in patients with IBD reveals decreased biodiversity of commensal bacteria, most notably the phyla Bacteroidetes and Firmicutes, including the clinically-relevant Faecalibacterium prausnitzii, and increased E. coli concentrations. VSL#3 is one probiotic preparation shown to be efficacious in certain clinical situations in small clinical trials. Further characterization of altered microbiota in patients with IBD and linking dysbiosis with host genetic alterations in immunoregulation, innate microbial killing and barrier function are critical, so that individualized treatments to increase beneficial commensals and their metabolic products (probiotic and prebiotic administration) and diminish deleterious species such as AIEC can be tailored for defined patient subsets.