Journal
JOURNAL OF MOLECULAR BIOLOGY
Volume 430, Issue 2, Pages 193-206Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2017.03.031
Keywords
epithelium; inflammasomes; NLRC4; NLRP3; interleukin-18
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Funding
- Swedish Research Council International Career Grant [2015-00635]
- Swiss National Science Foundation [SNF 310030_53074]
- SystemsX.ch
- Swiss Initiative in Systems Biology, RTD [51 RT-0_126008, 51RTP0_151029]
- Swedish Research Council [2015-00635] Funding Source: Swedish Research Council
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Inflammasome signaling impinges on the activation of inflammatory caspases (i.e., caspase-1 and caspase-4/5/11) and endows host cells with a sentinel system to sense microbial intrusion and thereby initiate appropriate immune responses. Lately, it has become evident that mammalian inflammasome-dependent responses to infection are not confined solely to cells of hematopoietic origin. Epithelial cells that line the body's mucosal surfaces use inflammasome signaling to sense and counteract pathogenic microorganisms that compromise barrier integrity. Many of the molecular mechanisms of epithelial inflammasome signaling remain unexplored. However, it now seems clear that epithelial inflammasome activation has a profound impact both on the infected cell itself and on its ability to communicate with other cell types of the mucosa. Here, we summarize current knowledge regarding the output of epithelial inflammasome activation during bacterial infection. Well-established downstream effects include epithelial cell death, release of soluble mediators, and subsequent recruitment of effector cell types, including NK cells, mast cells, and neutrophils, to sites of mucosal infection. We discuss the implications of recent findings for antibacterial defense in the mucosa and sketch out areas for future exploration. (C) 2017 Elsevier Ltd. All rights reserved.
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