Paneth cells directly sense gut commensals and maintain homeostasis at the intestinal host-microbial interface
Paneth cells directly sense gut commensals and maintain homeostasis at the intestinal host-microbial interface
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DOI：
10.1073/pnas.0808723105
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发表时间：
2008-12-30
影响因子：
11.1
通讯作者：
Hooper, Lora V.
中科院分区：
文献类型：
--
作者：
Vaishnava, Shipra;Behrendt, Cassie L.;Hooper, Lora V.
肠道上皮与大量的微生物群直接接触，但人们对上皮细胞如何保护宿主免受沉重的细菌负荷知之甚少。为了解决这个问题，我们研究了潘氏细胞，一个关键的小肠上皮细胞系。我们发现Paneth细胞通过细胞自主MyD88依赖性Toll样受体（TLR）激活直接感知肠道细菌，触发多种抗菌因子的表达。潘氏细胞是控制肠道细菌和病原菌穿透肠屏障的关键细胞。此外，Paneth细胞内在的MyD88信号传导限制了宿主组织的细菌渗透，揭示了上皮MyD88在维持肠道稳态中的作用。我们的研究结果表明，肠道上皮细胞积极的感觉肠道细菌，并在维持宿主微生物在粘膜界面的稳态发挥重要作用。
The intestinal epithelium is in direct contact with a vast microbiota, yet little is known about how epithelial cells defend the host against the heavy bacterial load. To address this question we studied Paneth cells, a key small intestinal epithelial lineage. We found that Paneth cells directly sense enteric bacteria through cell-autonomous MyD88-dependent toll-like receptor (TLR) activation, triggering expression of multiple antimicrobial factors. Paneth cells were essential for controlling intestinal barrier penetration by commensal and pathogenic bacteria. Furthermore, Paneth cell-intrinsic MyD88 signaling limited bacterial penetration of host tissues, revealing a role for epithelial MyD88 in maintaining intestinal homeostasis. Our findings establish that gut epithelia actively sense enteric bacteria and play an essential role in maintaining host-microbial homeostasis at the mucosal interface.