Prolonged administration of dexamethasone induces limited reactivation of visceral leishmaniosis in chronically infected BALB/c mice

Leishmania parasites persist in their vertebrate host after the treatment-i nduced clinical cure and in the asymptomatic infection. They confer resista nce to reinfection but represent a risk of occurrence of acute leishmaniosi s in immunosuppressed conditions. We examined the effects of prolonged dexa methasone administration on a chronic Leishmania infantum infection. Spleni c T cell populations from the long-term-infected BALB/c mice were reduced b y 55%, whereas those from uninfected controls were depleted by 85%. The abi lity of the remaining spleen cells to produce IL-2, IFN-gamma, IL-4 and TNF -alpha after in vitro specific stimulation decreased twofold, and the speci fic anti-leishmanial antibodies declined 3- to 5-fold. Liver, spleen and bo ne marrow are the main L. infantum targets in natural and experimental infe ctions. Three-fold increase of amastigote burden was evidenced in the splee n, after dexamethasone administration was prolonged for over 2 months. No r eactivation of Leishmania proliferation was disclosed in the liver and bone marrow. These results show a decreased sensitivity of splenic T cells to d examethasone in a chronic Leishmania infection and a distinct response of t he Leishmania-infected target organs to the dexamethasone-induced immunosup pression.