Absence of pro-survival A1 has no impact on inflammatory cell survival in vivo during acute lung inflammation and peritonitis
Abstract Inflammation is a natural defense 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 defense. The processes for eliminating inflammatory cells after pathogen clearance are critical in preventing sustained inflammation which can cause diverse pathologies. During chronic inflammation, 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 benefit. 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 homeostasis during inflammation and therefore does not constitute a therapeutic target for such morbidities.