Epithelial inflammasomes in the defense against Salmonella gut infection
•NAIP/NLRC4 and Caspase-4/11 inflammasomes restrict S.Tm infection of gut epithelium.•Importance of NAIP/NLRC4 versus Caspase-4/11 may shift between early and late infection.•Cell state and species-specific differences affect IEC inflammasome defense.•Interconnected inflammasome signalling may lead...
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| Published in | Current opinion in microbiology Vol. 59; pp. 86 - 94 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.02.2021
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| Subjects | |
| Online Access | Get full text |
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| Abstract | •NAIP/NLRC4 and Caspase-4/11 inflammasomes restrict S.Tm infection of gut epithelium.•Importance of NAIP/NLRC4 versus Caspase-4/11 may shift between early and late infection.•Cell state and species-specific differences affect IEC inflammasome defense.•Interconnected inflammasome signalling may lead to apoptotic or lytic IEC expulsion.
The gut epithelium prevents bacterial access to the host's tissues and coordinates a number of mucosal defenses. Here, we review the function of epithelial inflammasomes in the infected host and focus on their role in defense against Salmonella Typhimurium. This pathogen employs flagella to swim towards the epithelium and a type III secretion system (TTSS) to dock and invade intestinal epithelial cells. Flagella and TTSS components are recognized by the canonical NAIP/NLRC4 inflammasome, while LPS activates the non-canonical Caspase-4/11 inflammasome. The relative contributions of these inflammasomes, the activated cell death pathways and the elicited mucosal defenses are subject to environmental control and appear to change along the infection trajectory. It will be an important future task to explain how this may enable defense against the challenges imposed by diverse bacterial enteropathogens. |
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| AbstractList | The gut epithelium prevents bacterial access to the host's tissues and coordinates a number of mucosal defenses. Here, we review the function of epithelial inflammasomes in the infected host and focus on their role in defense against Salmonella Typhimurium. This pathogen employs flagella to swim towards the epithelium and a type III secretion system (TTSS) to dock and invade intestinal epithelial cells. Flagella and TTSS components are recognized by the canonical NAIP/NLRC4 inflammasome, while LPS activates the non-canonical Caspase-4/11 inflammasome. The relative contributions of these inflammasomes, the activated cell death pathways and the elicited mucosal defenses are subject to environmental control and appear to change along the infection trajectory. It will be an important future task to explain how this may enable defense against the challenges imposed by diverse bacterial enteropathogens. •NAIP/NLRC4 and Caspase-4/11 inflammasomes restrict S.Tm infection of gut epithelium.•Importance of NAIP/NLRC4 versus Caspase-4/11 may shift between early and late infection.•Cell state and species-specific differences affect IEC inflammasome defense.•Interconnected inflammasome signalling may lead to apoptotic or lytic IEC expulsion. The gut epithelium prevents bacterial access to the host's tissues and coordinates a number of mucosal defenses. Here, we review the function of epithelial inflammasomes in the infected host and focus on their role in defense against Salmonella Typhimurium. This pathogen employs flagella to swim towards the epithelium and a type III secretion system (TTSS) to dock and invade intestinal epithelial cells. Flagella and TTSS components are recognized by the canonical NAIP/NLRC4 inflammasome, while LPS activates the non-canonical Caspase-4/11 inflammasome. The relative contributions of these inflammasomes, the activated cell death pathways and the elicited mucosal defenses are subject to environmental control and appear to change along the infection trajectory. It will be an important future task to explain how this may enable defense against the challenges imposed by diverse bacterial enteropathogens. The gut epithelium prevents bacterial access to the host's tissues and coordinates a number of mucosal defenses. Here, we review the function of epithelial inflammasomes in the infected host and focus on their role in defense against Salmonella Typhimurium. This pathogen employs flagella to swim towards the epithelium and a type III secretion system (TTSS) to dock and invade intestinal epithelial cells. Flagella and TTSS components are recognized by the canonical NAIP/NLRC4 inflammasome, while LPS activates the non-canonical Caspase-4/11 inflammasome. The relative contributions of these inflammasomes, the activated cell death pathways and the elicited mucosal defenses are subject to environmental control and appear to change along the infection trajectory. It will be an important future task to explain how this may enable defense against the challenges imposed by diverse bacterial enteropathogens.The gut epithelium prevents bacterial access to the host's tissues and coordinates a number of mucosal defenses. Here, we review the function of epithelial inflammasomes in the infected host and focus on their role in defense against Salmonella Typhimurium. This pathogen employs flagella to swim towards the epithelium and a type III secretion system (TTSS) to dock and invade intestinal epithelial cells. Flagella and TTSS components are recognized by the canonical NAIP/NLRC4 inflammasome, while LPS activates the non-canonical Caspase-4/11 inflammasome. The relative contributions of these inflammasomes, the activated cell death pathways and the elicited mucosal defenses are subject to environmental control and appear to change along the infection trajectory. It will be an important future task to explain how this may enable defense against the challenges imposed by diverse bacterial enteropathogens. |
| Author | Sellin, Mikael E Fattinger, Stefan A Hardt, Wolf-Dietrich |
| Author_xml | – sequence: 1 givenname: Stefan A surname: Fattinger fullname: Fattinger, Stefan A organization: Institute of Microbiology, Department of Biology, ETH Zurich, Zurich, Switzerland – sequence: 2 givenname: Mikael E orcidid: 0000-0002-8355-0803 surname: Sellin fullname: Sellin, Mikael E organization: Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden – sequence: 3 givenname: Wolf-Dietrich surname: Hardt fullname: Hardt, Wolf-Dietrich email: hardt@micro.biol.ethz.ch organization: Institute of Microbiology, Department of Biology, ETH Zurich, Zurich, Switzerland |
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| Snippet | •NAIP/NLRC4 and Caspase-4/11 inflammasomes restrict S.Tm infection of gut epithelium.•Importance of NAIP/NLRC4 versus Caspase-4/11 may shift between early and... The gut epithelium prevents bacterial access to the host's tissues and coordinates a number of mucosal defenses. Here, we review the function of epithelial... |
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| SubjectTerms | cell death enteropathogens flagellum inflammasomes microbiology Salmonella Typhimurium |
| Title | Epithelial inflammasomes in the defense against Salmonella gut infection |
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