While the normal microbiota has been implicated as a critical defense against invading pathogens, the impact of enteropathogenic infection and host inflammation on intestinal microbial communities has not been elucidated. Using mouse models of Citrobacter rodentium, which closely mimics human diarrheal pathogens inducing host intestinal inflammation, and Campylobacter jejuni infection, as well as chemically and genetically induced models of intestinal inflammation, we demonstrate that host-mediated inflammation in response to an infecting agent, a chemical trigger, or genetic predisposition markedly alters the colonic microbial community. While eliminating a subset of indigenous microbiota, host-mediated inflammation supported the growth of either the resident or introduced aerobic bacteria, particularly of the Enterobacteriaceae family. Further, assault by an enteropathogen and host-mediated inflammation combined to significantly reduce the total numbers of resident colonic bacteria. These findings underscore the importance of intestinal microbial ecosystems in infectious colitis and noninfectious intestinal inflammatory conditions,such as inflammatory bowel disease.

中文翻译：

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宿主介导的炎症破坏了肠道菌群，并促进了肠杆菌科的过度生长。

虽然正常微生物群被认为是抵御入侵病原体的关键防御手段，但尚未阐明肠道致病菌感染和宿主炎症对肠道微生物群落的影响。使用紧密模拟人腹泻病原体诱导宿主肠道炎症和空肠弯曲菌感染的鼠疫柠檬酸杆菌的小鼠模型，以及化学和遗传诱导的肠道炎症模型，我们证明了宿主对炎症的反应是由媒介介导的。化学触发或遗传易感性会明显改变结肠微生物群落。在消除一部分本地微生物群的同时，宿主介导的炎症支持了常驻或引入的需氧细菌，特别是肠杆菌科的生长。进一步，肠病原菌的侵袭和宿主介导的炎症相结合，显着减少了常驻结肠细菌的总数。这些发现强调了肠道微生物生态系统在传染性结肠炎和非传染性肠道炎性疾病（例如炎性肠病）中的重要性。