| Literature DB >> 27460806 |
Anna-Karin Hermansson1, Ida Paciello1, Maria Lina Bernardini2,3.
Abstract
Shigella spp. are the causative agents of bacillary dysentery, leading to extensive mortality and morbidity worldwide. These facultative intracellular bacteria invade the epithelium of the colon and the rectum, inducing a severe inflammatory response from which the symptoms of the disease originate. Shigella are human pathogens able to manipulate and subvert the innate immune system surveillance. Shigella dampens inflammasome activation in epithelial cells. In infected macrophages, inflammasome activation and IL-1β and IL-18 release lead to massive neutrophil recruitment and greatly contribute to inflammation. Here, we describe how Shigella hijacks and finely tunes inflammasome activation in the different cell populations involved in pathogenesis: epithelial cells, macrophages, neutrophils, DCs, and B and T lymphocytes. Shigella emerges as a "sly" pathogen that switches on/off the inflammasome mechanisms in order to optimize the interaction with the host and establish a successful infection.Entities:
Keywords: Cell death; Dendritic cells; Epithelial cells; IL-18; IL-1β; Inflammasome; Inflammatory response; Lymphocytes; Macrophages; NLRC4; Neutrophils; Pyroptosis; Shigella; T3SS
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Year: 2016 PMID: 27460806 DOI: 10.1007/978-3-319-41171-2_5
Source DB: PubMed Journal: Curr Top Microbiol Immunol ISSN: 0070-217X Impact factor: 4.291