The Vibrio parahaemolyticus effector VopC mediates Cdc42‐dependent invasion of cultured cells but is not required for pathogenicity in an animal model of infection. (8th January 2014)

• Record Type: Journal Article
• Authors: Okada, Ryu; Zhou, Xiaohui; Hiyoshi, Hirotaka; Matsuda, Shigeaki; Chen, Xiang; Akeda, Yukihiro; Kashimoto, Takashige; Davis, Brigid M.; Iida, Tetsuya; Waldor, Matthew K.; Kodama, Toshio
• Is Part Of: Cellular microbiology. Volume 16:Number 6(2014:Jun.)
• Page Start: 938
• Page End: 947
• Publication Date: 2014-01-08
• 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.12252
• Languages: English
• ISSNs: 1462-5814

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p> <italic>V</italic> <italic>ibrio parahaemolyticus</italic> is a Gram‐negative marine bacterium that causes acute gastroenteritis in humans. The virulence of <italic>V</italic><italic>. parahaemolyticus</italic> is dependent upon a type III secretion system (T3SS2). One effector for T3SS2, VopC, is a homologue of the catalytic domain of cytotoxic necrotizing factor (CNF), and was recently reported to be a Rho family GTPase activator and to be linked to internalization of <italic>V</italic><italic>. parahaemolyticus</italic> by non‐phagocytic cultured cells. Here, we provide direct evidence that VopC deamidates Rac1 and CDC42, but not RhoA, <italic>in vivo</italic>. Our results alsosuggest that VopC, through its activation of Rac1, contributes to formation of actin stress fibres in infected cells. Invasion of host cells, which occurs at a low frequency, does not seem linked to Rac1 activation, but instead appears to require CDC42. Finally, using an infant rabbit model of <italic>V</italic><italic>. parahaemolyticus</italic> infection, we show that the virulence of <italic>V</italic><italic>. parahaemolyticus</italic> is not dependent upon VopC‐mediated invasion. Genetic inactivation of VopC did not impair intestinal colonization nor reduce signs of disease, including fluid accumulation, diarrhoea and tissue destruction. Thus, although VopC can promote host cell invasion, such internalization is not a critical step of the disease process, consistent with the traditional view of <italic>V</italic><italic>. parahaemolyticus</italic> as an extracellular pathogen.</p> </abstract>