Article ; Online: Cell death induced by NLRP3-palmitate axis impairs pulmonary damage tolerance and aggravates immunopathology during obesity-tuberculosis comorbidity.
2023 Volume 259, Issue 3, Page(s) 291–303
Abstract: A low-grade and persistent inflammation, which is the hallmark of obesity, requires the participation of NLRP3 and cell death. During Mycobacterium tuberculosis infection, NLRP3 signaling is important for bacterial killing by macrophages in vitro but was ...
Abstract | A low-grade and persistent inflammation, which is the hallmark of obesity, requires the participation of NLRP3 and cell death. During Mycobacterium tuberculosis infection, NLRP3 signaling is important for bacterial killing by macrophages in vitro but was shown to be dispensable for host protection in vivo. We hypothesized that during obesity-tuberculosis (TB) comorbidity, NLRP3 signaling might play a detrimental role by inducing excessive inflammation. We employed a model of high-fat-diet-induced obesity, followed by M. tuberculosis infection in C57BL/6 mice. Obese mice presented increased susceptibility to infection and pulmonary immunopathology compared to lean mice. Using treatment with NLRP3 antagonist and Nlrp3 |
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MeSH term(s) | Mice ; Animals ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Palmitates/metabolism ; Mice, Inbred C57BL ; Tuberculosis/pathology ; Mycobacterium tuberculosis ; Lung/pathology ; Inflammation/pathology ; Obesity/metabolism ; Cell Death ; Comorbidity |
Chemical Substances | NLR Family, Pyrin Domain-Containing 3 Protein ; Palmitates ; Nlrp3 protein, mouse |
Language | English |
Publishing date | 2023-01-03 |
Publishing country | England |
Document type | Journal Article ; Research Support, Non-U.S. Gov't |
ZDB-ID | 3119-7 |
ISSN | 1096-9896 ; 0022-3417 |
ISSN (online) | 1096-9896 |
ISSN | 0022-3417 |
DOI | 10.1002/path.6041 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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