Temesgen Ewunetu Andargie and Ermias Diro Ejara
Visceral leishmaniasis is a vector borne disease caused by Leishmania donovani complex. Pro- and anti-inflammatory cytokines play a key role in protecting from the pathogenesis of Leishmania infection, and their balance and dynamic changes may control or predict clinical outcome. Pro-inflammatory cytokines are created primarily to amplify inflammatory reactions; triggers the immune response to Leishmania infection. Even though this cytokine is necessary for a protective response, it may also cause excessive inflammation and collateral tissue damage. For this reason anti-inflammatory cytokines counteract the effects of pro-inflammatory cytokines to limit the inflammation present. However, an excessive down regulation of pro-inflammatory cytokines may favor disease progression. During VL/HIV co-infection, there is a decreased production of macrophage activating cytokines such as IFN-γ, IL-12, IL-15 and IL-18 and increased immunosuppressive cytokines like IL-4, IL-10 and TGF-β. Pro-inflammatory cytokine i.e. IL-6 and TNF-α also have been implicated in the pathogenesis of VL/HIV co-infection by inducing HIV replication. In peoples with VL and/or VL/HIV co-infection microbial translocation into the systemic circulation induces an intense pro-inflammatory response, which in turn activates lymphocyte. Thus, continuous and exaggerated activation causes exhaustion of the T-cell compartment and contributing to immunesuppression. Post kala-azar dermal leishmaniasis may also arise as a complication for VL following treatment. Its immunopathogenesis is not well understood, however, IL-10 is widely accepted as an immunosuppressive cytokine involved in the pathogenesis. Recently, IL-17 has contributed significantly to disease pathogenesis by inducing the production of TNF-α and NO.