Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut
Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut
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DOI：
10.1073/pnas.0307317101
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发表时间：
2004-02-17
影响因子：
11.1
通讯作者：
Fagarasan, S
中科院分区：
文献类型：
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作者：
Suzuki, K;Meek, B;Fagarasan, S
尽管肠道微生物群在身体防御中发挥着关键作用，但维持肠道微生物群稳态的机制仍然很大程度上未知。在活化诱导的胞苷脱氨酶 (AID) 缺乏的小鼠肠道中，超突变 lgA 的缺失被大量未突变 lgM 的存在以及防御素和血管生成素的正常表达水平部分补偿。我们在这里展示了 AID(-/-) 小鼠小肠中分段丝状细菌的显着且持续的扩张。 AID(-/-) 小鼠固有层 lgA 产生的重建恢复了肠道菌群的正常组成，并消除了免疫系统的局部和全身激活。结果表明，IgAs 的分泌而不是先天防御肽对于共生细菌菌群的调节至关重要，并且分段丝状细菌抗原是粘膜免疫系统的强烈刺激物。
The mechanism to maintain homeostasis of the gut microbiota remains largely unknown despite its critical role in the body defense. In the intestines of mice with deficiency of activation-induced cytidine deaminase (AID), the absence of hypermutated lgA is partially compensated for by the presence of large amounts of unmutated lgM and normal expression levels of defensins and angiogenins. We show here a predominant and persistent expansion of segmented filamentous bacteria throughout the small intestine of AID(-/-) mice. Reconstitution of lamina propria lgA production in AID(-/-) mice recovered the normal composition of gut flora and abolished the local and systemic activation of the immune system. The results indicate that secretions of lgAs rather than innate defense peptides are critical to regulation of commensal bacterial flora and that the segmented filamentous bacteria antigens are strong stimuli of the mucosal immune system.