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- Shiga toxins trigger the secretion of lysyl-tRNA synthetase to enhance proinflammatory responses
- Moo-Seung Lee; Haenaem Kwon; L T Nguyen; Eun Young Lee; C Y Lee; S H Choi; Myung Hee Kim
- Bibliographic Citation
- Journal of Microbiology and Biotechnology, vol. 26, no. 2, pp. 432-439
- Publication Year
- 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.
- Human lysyl-tRNA synthetaseProinflammatory mediatorShiga toxin
- Korea Soc-Assoc-Inst
- Appears in Collections:
- Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
Division of Biomedical Research > Microbiome Convergence Research Center > 1. Journal Articles
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