An In Vitro Investigation of the Effects of the Glucocorticoid on Leishmania major Amastigotes

Leishmaniasis is a vector-borne disease caused by Leishmania species. The transcription factor (NF-κB) activates and the innate immune system starts working when this parasite attacks macrophages. In addition, glucocorticoids increase nitric oxide (NO) and INFγ leads to the apoptosis of the cell by inhibiting the NF-κB activity. The aim of this study was the in vitro investigation of the effects of the glucocorticoids on Leishmania major amastigotes.

Leishmania major was produced in a massive volume. Then, promastigotes penetrated into macrophages and converted to amastigotes by adding promastigotes to the J774 mouse macrophage cell line and providing appropriate conditions. Next, the infected macrophages with L. major parasite were treated with different concentrations of prednisolone and mometasone. After 24 and 48 hours, the effect of the drugs was evaluated based on the average number of amastigotes in the infected macrophages. In addition, the amount of NO and the mean interleukin 12 (IL-12) level secreted by the infected macrophages treated with different concentrations of drugs were measured by Griess reagent and ELISA reader, respectively.

The average number of amastigotes in the infected macrophages treated with different concentrations of the drug was significantly different from the control group. Further, the amount of NO and the mean level of IL-12 secreted by infected macrophages had a direct and significant relationship with different concentrations of drugs, but the results of Tukey post hoc test showed that the reduction in the number of promastigotes was not time-dependent.

In general, prednisolone and mometasone stimulated macrophages increased the IL-12 levels and NO secretion and finally decreased the number of parasites in infected macrophages.