Cytosolic recognition of flagellin by mouse macrophages restricts Legionella pneumophila infection.
Cytosolic recognition of flagellin by mouse macrophages restricts Legionella pneumophila infection.
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小鼠巨噬细胞对鞭毛蛋白的胞质识别限制了肺炎军团菌感染。
DOI：
10.1084/jem.20051659
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发表时间：
2006-04-17
期刊：
影响因子：
--
通讯作者：
Swanson MS
中科院分区：
文献类型：
--
作者：
Molofsky AB;Byrne BG;Whitfield NN;Madigan CA;Fuse ET;Tateda K;Swanson MS
To restrict infection by Legionella pneumophila, mouse macrophages require Naip5, a member of the nucleotide-binding oligomerization domain leucine-rich repeat family of pattern recognition receptors, which detect cytoplasmic microbial products. We report that mouse macrophages restricted L. pneumophila replication and initiated a proinflammatory program of cell death when flagellin contaminated their cytosol. Nuclear condensation, membrane permeability, and interleukin-1β secretion were triggered by type IV secretion-competent bacteria that encode flagellin. The macrophage response to L. pneumophila was independent of Toll-like receptor signaling but correlated with Naip5 function and required caspase 1 activity. The L. pneumophila type IV secretion system provided only pore-forming activity because listeriolysin O of Listeria monocytogenes could substitute for its contribution. Flagellin monomers appeared to trigger the macrophage response from perforated phagosomes: once heated to disassemble filaments, flagellin triggered cell death but native flagellar preparations did not. Flagellin made L. pneumophila vulnerable to innate immune mechanisms because Naip5+ macrophages restricted the growth of virulent microbes, but flagellin mutants replicated freely. Likewise, after intratracheal inoculation of Naip5+ mice, the yield of L. pneumophila in the lungs declined, whereas the burden of flagellin mutants increased. Accordingly, macrophages respond to cytosolic flagellin by a mechanism that requires Naip5 and caspase 1 to restrict bacterial replication and release proinflammatory cytokines that control L. pneumophila infection.
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影响因子：
4.8
作者：
Garcia-Calvo, M;Peterson, EP;Thornberry, NA
通讯作者：
Thornberry, NA
一种常见的主导TLR5停止密码子多态性废除了鞭毛蛋白信号传导，并与对军团疾病的易感性有关。
影响因子：
15.3
作者：
Hawn, TR;Verbon, A;Lettinga, KD;Zhao, LP;Li, SS;Laws, RJ;Skerrett, SJ;Beutler, B;Schroeder, L;Nachman, A;Ozinsky, A;Smith, KD;Aderem, A
通讯作者：
Aderem, A
影响因子：
3.4
作者：
Amer, AO;Swanson, MS
通讯作者：
Swanson, MS
影响因子：
4.8
作者：
Davoodi, J;Lin, L;MacKenzie, AE
通讯作者：
MacKenzie, AE
DOI：
10.1073/pnas.0502040102
发表时间：
2005-06-28
影响因子：
11.1
作者：
Andersen-Nissen, E;Smith, KD;Aderem, A
通讯作者：
Aderem, A