Open AccessDexamethasone modulates Salmonella enterica serovar Typhimurium infection in vivo independently of the glucocorticoid‐inducible protein annexin‐A1
Author(s) -
Smyth Tomoko,
Tötemeyer Sabine,
Haugland Sean,
Willers Chrissie,
Peters Sarah,
Maskell Duncan,
Bryant Clare
Publication year - 2008
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2008.00485.x
Subject(s) - salmonella enterica , dexamethasone , lipopolysaccharide , biology , glucocorticoid , microbiology and biotechnology , annexin a1 , salmonella , proinflammatory cytokine , inflammation , in vivo , immunology , endocrinology , annexin , bacteria , flow cytometry , genetics
Salmonella enterica serovar Typhimurium ( S. Typhimurium) infection causes an inflammatory response through activation of Toll‐like receptor 4 by lipopolysaccharide. Dexamethasone, a glucocorticoid analogue, suppresses inflammatory responses by many mechanisms including inhibition of the lipopolysaccharide‐induced production of proinflammatory mediators. There is little information on the effect of glucocorticoids on murine salmonellosis. In this study, we treated susceptible BALB/c mice by subcutaneous implantation of slow‐release dexamethasone pellets before infection with S. Typhimurium. Dexamethasone promotes bacterial growth early in infection and induces a dose‐dependent increase in bacterial growth within mouse livers and spleens. The bacterial load in organs from infected placebo‐treated mice was lower than that in dexamethasone‐treated mice. Glucocorticoids inhibit lipopolysaccharide‐induced inflammation partially through the steroid‐inducible protein annexin‐A1 (ANXA1). Infection of wild‐type and ANXA1 knock‐out mice with S. Typhimurium led to similar organ bacterial loads. ANXA1 also did not affect the bacterial load in organs from infected dexamethasone‐treated mice. This suggests that glucocorticoids, independently of ANXA1, accelerate S. Typhimurium growth in vivo in susceptible BALB/c mice.