Leishmania is an obligate intracellular parasite uses low pH phagolysosomal compartments of host macrophages as their final abode. IL-1β is a pro inflammatory cytokine, which is secreted by immune cells to trigger inflammation and this has been found profoundly in the lesions caused by Leishmania pathogens. But the specific role of this cytokine on host cell macrophages during infection has not been fully explored. Here in, we have showed that prolonged exposure of IL-1β on macrophages increases the parasite burden. Pre-treatment of bone marrow derived macrophages (BMDM) with IL-1β also generates significantly higher amount of anti-inflammatory cytokine IL-10. As IL-10 plays crucial role in the establishment of infection, enhanced production of IL-10 observed upon IL-1β treatment could contribute to the progression of the disease. By quantifying the production of Nitric oxide (NO), we further report that the pretreatment of IL-1β fails to produce the nitric oxide. By measuring the footpad thickness in two different mice strains of differential susceptibility we showed IL-1β treatment increases parasitic burden. As our results shows that the exposure of IL-1β helps in disease progression, IL-1β signalling may be an attractive target for future therapeutic intervention.
Keywords: IL-10; IL-1β; Parasitic burden.
Copyright © 2018. Published by Elsevier Ltd.