Absence of pro-survival A1 has no impact on inflammatory cell survival in vivo during acute lung inflammation and peritonitis.

Autor: Gangoda L; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia.; La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia., Schenk RL; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia., Best SA; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia., Nedeva C; La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia., Louis C; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia., D'Silva DB; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia., Fairfax K; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia.; Menzies Institute for Medical Research, University of Tasmania, Hobart, TAS, Australia., Jarnicki AG; Department of Biochemistry and Pharmacology, University of Melbourne, Parkville, VIC, Australia., Puthalakath H; La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia., Sutherland KD; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia., Strasser A; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia., Herold MJ; The Walter and Eliza Hall Institute of Medical Research (WEHI), Melbourne, VIC, Australia. herold@wehi.edu.au.; Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia. herold@wehi.edu.au.
Jazyk: angličtina
Zdroj: Cell death and differentiation [Cell Death Differ] 2022 Jan; Vol. 29 (1), pp. 96-104. Date of Electronic Publication: 2021 Jul 24.
DOI: 10.1038/s41418-021-00839-3
Abstrakt: Inflammation is a natural defence mechanism of the body to protect against pathogens. It is induced by immune cells, such as macrophages and neutrophils, which are rapidly recruited to the site of infection, mediating host defence. The processes for eliminating inflammatory cells after pathogen clearance are critical in preventing sustained inflammation, which can instigate diverse pathologies. During chronic inflammation, the excessive and uncontrollable activity of the immune system can cause extensive tissue damage. New therapies aimed at preventing this over-activity of the immune system could have major clinical benefits. Here, we investigated the role of the pro-survival Bcl-2 family member A1 in the survival of inflammatory cells under normal and inflammatory conditions using murine models of lung and peritoneal inflammation. Despite the robust upregulation of A1 protein levels in wild-type cells upon induction of inflammation, the survival of inflammatory cells was not impacted in A1-deficient mice compared to wild-type controls. These findings indicate that A1 does not play a major role in immune cell homoeostasis during inflammation and therefore does not constitute an attractive therapeutic target for such morbidities.
(© 2021. The Author(s), under exclusive licence to ADMC Associazione Differenziamento e Morte Cellulare.)
Databáze: MEDLINE
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