Leptospiral outer membrane protein LMB216 is involved in enhancement of phagocytic uptake by macrophages. (9th April 2014)

• Record Type: Journal Article
• Authors: Toma, Claudia; Murray, Gerald L.; Nohara, Toshitsugu; Mizuyama, Masaru; Koizumi, Nobuo; Adler, Ben; Suzuki, Toshihiko
• Is Part Of: Cellular microbiology. Volume 16:Number 9(2014:Sep.)
• Page Start: 1366
• Page End: 1377
• Publication Date: 2014-04-09
• Subjects: Microbiology -- Periodicals; Cytology -- Periodicals; Host-parasite relationships -- Periodicals; Microbiology -- Periodicals; Cells -- Periodicals; Microbiologie -- Périodiques; Microbiologie; Relation hôte-parasite; Cytologie; Cellule; Réponse cellulaire; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); 579.05
• DOI: 10.1111/cmi.12296
• Languages: English
• ISSNs: 1462-5814

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p> <italic>L</italic> <italic>eptospira interrogans</italic> 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 <italic>in vivo</italic> 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 (<underline>l</underline>eptospiral <underline>i</underline>mmuno<underline>g</underline>lobulin‐like protein <underline>B</underline>) 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.</p> </abstract>