T3SS effector VopL inhibits the host ROS response, promoting the intracellular survival of Vibrio parahaemolyticus

PLoS Pathogens

Dor Salomon¹  Kim Orth¹  Marcela de Souza Santos¹ 

[1] Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas, United States of America

关键词: Actins;    Cell membranes;    Caco-2 cells;    Intracellular pathogens;    Host cells;    Cytoskeleton;    Superoxides;    Cytosol;   

DOI  :  10.1371/journal.ppat.1006438

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

The production of antimicrobial reactive oxygen species by the nicotinamide dinucleotide phosphate (NADPH) oxidase complex is an important mechanism for control of invading pathogens. Herein, we show that the gastrointestinal pathogen Vibrio parahaemolyticus counteracts reactive oxygen species (ROS) production using the Type III Secretion System 2 (T3SS2) effector VopL. In the absence of VopL, intracellular V. parahaemolyticus undergoes ROS-dependent filamentation, with concurrent limited growth. During infection, VopL assembles actin into non-functional filaments resulting in a dysfunctional actin cytoskeleton that can no longer mediate the assembly of the NADPH oxidase at the cell membrane, thereby limiting ROS production. This is the first example of how a T3SS2 effector contributes to the intracellular survival of V. parahaemolyticus, supporting the establishment of a protective intracellular replicative niche.

【 授权许可】

CC BY