Listerial invasion protein internalin B promotes entry into ileal Peyer's patches in vivo
Listerial invasion protein internalin B promotes entry into ileal Peyer's patches in vivo
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DOI：
10.1111/j.1348-0421.2010.00292.x
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发表时间：
2011-02-01
影响因子：
2.6
通讯作者：
Koyasu, Shigeo
中科院分区：
文献类型：
--
作者：
Chiba, Sayuri;Nagai, Takeshi;Koyasu, Shigeo
单核细胞增多性李斯特菌（Listeria monocytogenes，Lm）通过胞内侵袭蛋白（internalins）侵入宿主肠道。本文报道了内分泌蛋白A（InlA）和内分泌蛋白B（InlB）的体内作用。胃内（i.g.）施用和用Δ inlB-Lm的连接环测定证明，缺乏InlB显著减弱Lm侵入各种器官的能力。另一方面，表达具有两个取代S192 N和Y369 S的突变体InlA的InlAm-Lm（其已被报道增加InlA对小鼠E-钙粘蛋白的亲和力）根据连接环和i.g.感染测定。Lm优先通过M细胞进入回肠派尔集合淋巴结（PP），并且Δ inlB-Lm显示出通过这些细胞侵入的能力严重降低。本研究结果揭示了InlB的重要性，它加速了体内回肠PP上的M细胞的侵袭。
Listeria monocytogenes (Lm) invades the host intestine using listerial invasion proteins, internalins. The in vivo role of internalin A (InlA) and internalin B (InlB) is reported here. Intragastric (i.g.) administration and ligated loop assays with delta inlB-Lm demonstrated that a lack of InlB significantly attenuates the invasive ability of Lm into various organs. On the other hand, InlAm-Lm expressing a mutant InlA with two substitutions, S192N and Y369S, which has been reported to increase the affinity of InlA to mouse E-cadherin, resulted in little increase in intestinal infection according to both ligated loop and i.g. infection assays. Lm preferentially enters ileal Peyer's patch (PP) via M cells and delta inlB-Lm showed severely reduced ability to invade though these cells. The present results reveal the importance of InlB, which accelerates listerial invasion into M cells on ileal PPs in vivo.