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李斯特菌侵袭蛋白内毒素 B 促进体内回肠派尔集合淋巴结的入侵。

Listerial invasion protein internalin B promotes entry into ileal Peyer's patches in vivo.

机构信息

Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.

出版信息

Microbiol Immunol. 2011 Feb;55(2):123-9. doi: 10.1111/j.1348-0421.2010.00292.x.

Abstract

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 ΔinlB-Lm demonstrated that a lack of InlB significantly attenuates the invasive ability of Lm into various organs. On the other hand, InlA(m)-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 ΔinlB-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.

摘要

李斯特菌(Lm)使用李斯特菌侵袭蛋白(内毒素)侵袭宿主肠道。本文报道了内毒素 A(InlA)和内毒素 B(InlB)的体内作用。通过胃内(i.g.)给药和结扎环试验用ΔinlB-Lm 表明,缺乏 InlB 可显著降低 Lm 侵袭各种器官的能力。另一方面,表达突变体 InlA 的 InlA(m)-Lm,其 InlA 有两个取代,S192N 和 Y369S,据报道,该取代可增加 InlA 与小鼠 E-钙黏蛋白的亲和力,根据结扎环和 i.g. 感染试验,其在肠道感染中的增加作用不大。Lm 优先通过 M 细胞进入回肠派尔集合淋巴结(PP),而ΔinlB-Lm 则显示出通过这些细胞侵袭的能力严重降低。本研究结果揭示了 InlB 的重要性,InlB 可加速李斯特菌在体内通过回肠派尔集合淋巴结的 M 细胞侵袭。

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