Shiga toxins expressed by human pathogenic bacteria induce immune responses in host cells = 숙주내에서 면역반응을 유도하는 인간병원체 박테리아로부터 배출되는 시가독소

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Title
Shiga toxins expressed by human pathogenic bacteria induce immune responses in host cells = 숙주내에서 면역반응을 유도하는 인간병원체 박테리아로부터 배출되는 시가독소
Author(s)
Moo Seung LeeMyung Hee Kim; V L Tesh
Bibliographic Citation
Journal of Microbiology, vol. 51, no. 6, pp. 724-730
Publication Year
2013
Abstract
Shiga toxins are a family of genetically and structurally related toxins that are the primary virulence factors produced by the bacterial pathogens Shigella dysenteriae serotype 1 and certain Escherichia coli strains. The toxins are multifunctional proteins inducing protein biosynthesis inhibition, ribotoxic and ER stress responses, apoptosis, autophagy, and inflammatory cytokine and chemokine production. The regulated induction of inflammatory responses is key to minimizing damage upon injury or pathogen-mediated infections, requiring the concerted activation of multiple signaling pathways to control cytokine/chemokine expression. Activation of host cell signaling cascades is essential for Shiga toxin-mediated proinflammatory responses and the contribution of the toxins to virulence. Many studies have been reported defining the inflammatory response to Shiga toxins in vivo and in vitro, including production and secretion of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), macrophage inflammatory protein-1α/β (MIP-1α/β), macrophage chemoattractant monocyte chemoattractant protein 1 (MCP-1), interleukin 8 (IL-8), interleukin 6 (IL-6), and Groβ. These cytokines and chemokines may contribute to damage in the colon and development of life threatening conditions such as acute renal failure (hemolytic uremic syndrome) and neurological abnormalities. In this review, we summarize recent findings in Shiga toxin-mediated inflammatory responses by different types of cells in vitro and in animal models. Signaling pathways involved in the inflammatory responses are briefly reviewed.
Keyword
animal modelHUSinflammatory responseShiga toxinsignaling
ISSN
1225-8873
Publisher
Microbiological Society Korea
DOI
http://dx.doi.org/10.1007/s12275-013-3429-6
Type
Article
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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