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首页> 外文期刊>Cell Host & Microbe >The beta(2) Integrin Mac-1 Induces Protective LC3-Associated Phagocytosis of Listeria monocytogenes
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The beta(2) Integrin Mac-1 Induces Protective LC3-Associated Phagocytosis of Listeria monocytogenes

机译：β（2）整合蛋白MAC-1诱导李斯特菌单核细胞增生的保护剂LC3相关吞噬作用

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摘要

The intracellular pathogen Listeria monocytogenes (L.m.) is targeted by the autophagic machinery, but the molecular mechanisms involved and consequences for anti-listerial immunity remain enigmatic. Here, we demonstrate that L.m. infection of macrophages in vivo exclusively evokes LC3-associated phagocytosis (LAP), but not canonical autophagy, and that targeting of L.m. by LAP is required for anti-listerial immunity. The pathway leading to LAP induction in response to L.m. infection emanates from the beta(2) integrin Mac-1 (CR3, integrin alpha(M)beta(2)), a receptor recognizing diverse microbial ligands. Interaction of L.m. with Mac-1 induces acid sphingomye-linase-mediated changes in membrane lipid composition that facilitate assembly and activation of the phagocyte NAPDH oxidase Nox2. Nox2-derived reactive oxygen species then trigger LC3 recruitment to L.m.-containing phagosomes by LAP. By promoting fusion of L.m.-containing phagosomes with lysosomes, LAP increases exposure of L.m. to bactericidal acid hydrolases, thereby enhancing anti-listerial activity of macrophages and immunity of mice.
机译：细胞内病原体李斯特菌单核细胞增生（L.M.）由自噬机械靶向，但涉及的分子机制和对抗脑梗润的后果仍然是神秘的。在这里，我们证明了l.m.体内感染巨噬细胞专门唤起LC3相关的吞噬作用（圈），但不是规范自噬，并瞄准l.m。通过LAP进行抗议疫苗。途径导致搭接响应LAP的诱导。感染来自β（2）整合蛋白MAC-1（CR3，整合蛋白α（m）β（2）），受体识别不同的微生物配体。 L.M的相互作用使用MAC-1诱导酸鞘磷脂 - 型膜血液组合物的变化，其促进吞噬细胞NAPDH氧化酶NOx2的组装和活化。然后NOx2衍生的反应性氧物种然后将LC3募集到LAP的LAP募集。通过膝盖含有吞噬物质。通过促进L.M的融合。含有溶酶体的吞噬体，LAP增加了L.M的曝光。对于杀菌酸水解酶，从而提高小鼠巨噬细胞和免疫的抗脑卒中活性。

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