SRC3 deficiency exacerbates lipopolysaccharide-induced acute respiratory distress syndrome in mice.

Abstract

Acute respiratory distress syndrome (ARDS) is a severe disease. Inflammation is the key element implicated in ARDS. Steroid receptor coactivator 3 (SRC3), a coactivator protein for transcription, is involved in regulation of inflammatory response. Here we explored the potential roles of SRC3 in ARDS. We utilized the SRC3 deficient (SRC3) mice and established the lipopolysaccharides (LPS)-induced ARDS model. The mortality, lung injury, leucocytes infiltration and inflammatory cytokine production were compared between wild type (WT) and SRC3mice. The NF-κB activation in lung of WT and SRC3mice was measured. After LPS treatment, SRC3mice had higher mortality and more severe lung damage than WT mice. LPS-treated SRC3mice had more leucocytes infiltration and upregulated inflammatory cytokine production. LPS-treated SRC3mice had elevated NF-κB activation. SRC3mice had exacerbated ARDS in LPS-treated mice.