Murine colitis is mediated by vimentin.

Mor-Vaknin N, Legendre M, Yu Y, Serezani CH, Garg SK, Jatzek A, Swanson MD, Gonzalez-Hernandez MJ, Teitz-Tennenbaum S, Punturieri A, Engleberg NC, Banerjee R, Peters-Golden M, Kao JY, Markovitz DM
Sci Rep. 2013 3: 1045

PMID: 23304436 · PMCID: PMC3540396 · DOI:10.1038/srep01045

Vimentin, an abundant intermediate filament protein, presumably has an important role in stabilizing intracellular architecture, but its function is otherwise poorly understood. In a vimentin knockout (Vim KO) mouse model, we note that Vim KO mice challenged with intraperitoneal Escherichia coli control bacterial infection better than do wild-type (WT) mice. In vitro, Vim KO phagocytes show significantly increased capacity to mediate bacterial killing by abundant production of reactive oxygen species (ROS) and nitric oxides, likely due to interactions with the p47phox active subunit of NADPH oxidase. In acute colitis induced by dextran sodium sulfate (DSS), Vim KO mice develop significantly less gut inflammation than do WT mice. Further, Vim KO mice have markedly decreased bacterial extravasation in the setting of DSS-induced acute colitis, consistent with decreased intestinal disease. Our results suggest that vimentin impedes bacterial killing and production of ROS, thereby contributing to the pathogenesis of acute colitis.

MeSH Terms (14)

Animals Colitis Dextran Sulfate Escherichia coli Macrophages Mice Mice, Knockout NADPH Oxidases Nitric Oxide Phagocytosis Reactive Oxygen Species RNA, Small Interfering RNA Interference Vimentin

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