Infection is the outcome of a contest between a pathogen and its host. In the disease leishmaniasis, the causative protozoan parasites are harbored inside the macrophages. Leishmania species adapt strategies to make the infection chronic, keeping a balance between their own and the host's defense so as to establish an environment that is favorable for survival and propagation. Activation of peroxisome proliferator-activated receptor (PPAR) is one of the tactics used. This ligand-activated nuclear factor curbs inflammation to protect the host from excessive injuries by setting a limit to its destructive force. In this paper, we report the interaction of host PPARs and the pathogen for visceral leishmaniasis, Leishmania donovani, in vivo and in vitro. PPAR expression is induced by parasitic infection. Leishmanial activation of PPARγ promotes survival, whereas blockade of PPARγ facilitates removal of the parasite. Thus, Leishmania parasites harness PPARγ to increase infectivity. 1. Leishmaniasis Leishmaniasis is caused by parasitic protozoa of the genus Leishmania. The disease is found worldwide, with an estimated prevalence of 12 million cases, 50,000 annual deaths, and 350 millions of the world’s population at risk [1]. Leishmania has two stages in its life cycle: flagellated promastigotes that live within the alimentary canal of the insect vector and amastigotes that multiply within the phagolysosomes of mammalian macrophages. Infected female sandflies introduce saliva and promastigotes into the mammalian host during blood meals. The promastigotes are taken by leukocytes and differentiate into intracellular amastigotes within the macrophages. Then, infected macrophages carry the parasites to different organs. Over twenty species are known to infect humans. The cutaneous species reside and multiply within the skin tissue, whereas the visceral species predominantly accumulate in the liver, spleen, and bone marrow. These diverse species cause different clinical manifestations, varying from self-healing or metastasizing skin lesions to enlargement of visceral organs including the liver and spleen. The disease symptoms are classified as cutaneous, mucocutaneous, or visceral leishmaniasis. 2. Resistance versus Susceptibility Immunity against all species of Leishmania uniformly relies on a type 1 immune response that produces interferon γ (IFNγ). Produced by T helper 1 cells, IFNγ activates macrophages to generate nitric oxide (NO), a free radical that can kill Leishmania. Type 2 immune response, on the other hand, is ineffective [2]. Production of
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