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首页> 外文期刊>Scientific reports. >A gut pathobiont synergizes with the microbiota to instigate inflammatory disease marked by immunoreactivity against other symbionts but not itself
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A gut pathobiont synergizes with the microbiota to instigate inflammatory disease marked by immunoreactivity against other symbionts but not itself

机译：肠道致病菌与微生物群协同作用，引发以针对其他共生体的免疫反应为特征的炎症性疾病，但不针对自身

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Inflammatory bowel diseases (IBD) are likely driven by aberrant immune responses directed against the resident microbiota. Although IBD is commonly associated with a dysbiotic microbiota enriched in putative pathobionts, the etiological agents of IBD remain unknown. Using a pathobiont-induced intestinal inflammation model and a defined bacterial community, we provide new insights into the immune-microbiota interactions during disease. In?this model system, the pathobiont Helicobacter bilis instigates disease following sub-pathological dextran sulfate sodium treatment. We show that H. bilis causes mild inflammation in mono-associated mice, but severe disease in the presence of a microbiota, demonstrating synergy between the pathobiont and microbiota in exacerbating pathology. Remarkably, inflammation depends on the presence of H. bilis, but is marked by a predominant Th17 response against specific members of the microbiota and not the pathobiont, even upon the removal of the most immune-dominant taxa. Neither increases in pathobiont burden nor unique changes in immune-targeted microbiota member abundances are observed during disease. Collectively, our findings demonstrate that a pathobiont instigates inflammation without being the primary target of a Th17 response or by altering the microbiota community structure. Moreover, our findings point toward monitoring pathobiont-induced changes in microbiota immune targeting as a new concept in IBD diagnotics.
机译：针对肠道菌群的异常免疫反应可能导致炎症性肠病（IBD）。尽管IBD通常与假定的病原体富集的营养不良微生物群有关，但IBD的病原体仍然未知。使用病原菌诱导的肠道炎症模型和定义的细菌群落，我们提供了疾病期间免疫微生物群相互作用的新见解。在该模型系统中，病原菌Helicobacter bilis在亚病理性葡聚糖硫酸钠处理后引发疾病。我们显示，H。bilis会在单关联小鼠中引起轻度炎症，但在存在微生物群的情况下会导致严重疾病，这表明病原菌和微生物群之间的协同作用加剧了病理。值得注意的是，炎症取决于H. bilis的存在，但以针对微生物群的特定成员而不是病原生物的Th17反应为主，即使去除了免疫力最强的分类单元也是如此。在疾病期间，既未观察到病态负担增加，也未观察到免疫目标微生物群成员丰度的独特变化。总体而言，我们的研究结果表明，病原菌能够引发炎症，而不会成为Th17反应的主要靶标，也不会改变微生物群的结构。此外，我们的发现指向监测病原体诱导的微生物群免疫靶向的变化，作为IBD诊断的新概念。

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