Effects of glucocorticoids in Leishmania major infection

Leishmania parasites activate NF-κB which induces Th2 expression and inactivates Th1 genes thus subverting the host defense response and promotes the survival and development of the parasite in macrophages. Macrophages were treated artificially with glucocorticoids and incubated with Leishmania promastigotes. Interleukin 1 β, Tumor necrosis factor- α and inhibitory nitric oxide synthase gene levels were measured using real time PCR and parasite development monitored in vitro. Tumor necrosis factor- α and nitric oxide synthase genes were down-regulated and Interleukin 1 β upregulated in macrophages treated with dexamethasone and hydrocortisone drugs when compared to those treated with lipopolysaccharide and untreated. Dexamethasone treated macrophages had significantly low number of amastigotes compared to hydrocortisone and lipopolysaccharide (p=0.0006). Dexamethasone showed high reduction of infection rates in macrophages as compared to hydrocortisone and lipopolysaccharide treated macrophages, however not significant (p=0.054). With further clinical studies in humans, dexamethasone may be used in the control of leishmaniasis.