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http://dx.doi.org/10.4014/jmb.1511.11056

Shiga Toxins Trigger the Secretion of Lysyl-tRNA Synthetase to Enhance Proinflammatory Responses  

Lee, Moo-Seung (Infection and Immunity Research Center, Korea Research Institute of Bioscience and Biotechnology)
Kwon, Haenaem (Infection and Immunity Research Center, Korea Research Institute of Bioscience and Biotechnology)
Nguyen, Loi T. (Infection and Immunity Research Center, Korea Research Institute of Bioscience and Biotechnology)
Lee, Eun-Young (Infection and Immunity Research Center, Korea Research Institute of Bioscience and Biotechnology)
Lee, Chan Yong (Department of Biochemistry, Chungnam National University)
Choi, Sang Ho (Department of Agricultural Biotechnology, Seoul National University)
Kim, Myung Hee (Infection and Immunity Research Center, Korea Research Institute of Bioscience and Biotechnology)
Publication Information
Journal of Microbiology and Biotechnology / v.26, no.2, 2016 , pp. 432-439 More about this Journal
Abstract
Shiga toxins (Stxs) produced by Shiga toxin-producing Escherichia coli (STEC) strains are major virulence factors that cause fatal systemic complications, such as hemolytic uremic syndrome and disruption of the central nervous system. Although numerous studies report proinflammatory responses to Stx type 1 (Stx1) or Stx type 2 (Stx2) both in vivo and in vitro, none have examined dynamic immune regulation involving cytokines and/or unknown inflammatory mediators during intoxication. Here, we showed that enzymatically active Stxs trigger the dissociation of lysyl-tRNA synthetase (KRS) from the multi-aminoacyl-tRNA synthetase complex in human macrophage-like differentiated THP-1 cells and its subsequent secretion. The secreted KRS acted to increase the production of proinflammatory cytokines and chemokines. Thus, KRS may be one of the key factors that mediate transduction of inflammatory signals in the STEC-infected host.
Keywords
Shiga toxin; human lysyl-tRNA synthetase; proinflammatory mediator;
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