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钩端螺旋体外膜蛋白LMB216参与增强巨噬细胞的吞噬摄取。

Leptospiral outer membrane protein LMB216 is involved in enhancement of phagocytic uptake by macrophages.

作者信息

Toma Claudia, Murray Gerald L, Nohara Toshitsugu, Mizuyama Masaru, Koizumi Nobuo, Adler Ben, Suzuki Toshihiko

机构信息

Department of Molecular Bacteriology and Immunology, Graduate School of Medicine, University of the Ryukyus, Okinawa, 903-0215, Japan.

出版信息

Cell Microbiol. 2014 Sep;16(9):1366-77. doi: 10.1111/cmi.12296. Epub 2014 Apr 9.

Abstract

Leptospira interrogans is responsible for the zoonotic disease leptospirosis. The pathogenic mechanisms of this spirochaete remain poorly understood; however, virulence has been correlated with increased phagocytic uptake and survival within macrophages. Leptospiral outer membrane proteins are thought to be responsible for persistence in vivo via interaction with specific host components. In this study, we analysed the transcriptional profile of a virulent strain and its culture-attenuated derivative strain to identify bacterial factors that may be involved in pathogenesis. Two outer membrane proteins, LMB216 and LigB (leptospiral immunoglobulin-like protein B) were downregulated more than 10-fold in the culture-attenuated strain. We show that both proteins play a role in leptospiral uptake by macrophages and that LMB216, as well as LigB, enhances the binding of leptospires to fibronectin. Taken together, our results indicate that LMB216 plays a role in pathogen interaction with host molecule/s, which may contribute to pathogenesis of leptospirosis.

摘要

问号钩端螺旋体是导致人畜共患病钩端螺旋体病的病原体。这种螺旋体的致病机制仍知之甚少;然而,毒力与巨噬细胞内吞噬摄取增加和存活相关。钩端螺旋体外膜蛋白被认为通过与特定宿主成分相互作用而在体内持续存在。在本研究中,我们分析了一株强毒株及其培养减毒株的转录谱,以鉴定可能参与发病机制的细菌因子。两种外膜蛋白LMB216和LigB(钩端螺旋体免疫球蛋白样蛋白B)在培养减毒株中下调超过10倍。我们表明这两种蛋白在巨噬细胞摄取钩端螺旋体中发挥作用,并且LMB216以及LigB增强钩端螺旋体与纤连蛋白的结合。综上所述,我们的结果表明LMB216在病原体与宿主分子的相互作用中发挥作用,这可能有助于钩端螺旋体病的发病机制。

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