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 SRC3-/- mice. The NF-κB activation in lung of WT and SRC3-/- mice was measured. After LPS treatment, SRC3-/- mice had higher mortality and more severe lung damage than WT mice. LPS-treated SRC3-/- mice had more leucocytes infiltration and upregulated inflammatory cytokine production. LPS-treated SRC3-/- mice had elevated NF-κB activation. SRC3-/- mice had exacerbated ARDS in LPS-treated mice.