Lipid Mediators in Host-Pathogen Interactions during Leishmania Infection: Friends or Foes?

Lipid mediators can control the inflammatory response in infectious diseases, including leishmaniasis. However, these mediators may promote antagonistic roles in the Leishmania-host interaction depending on the species involved in the infection. Herein, we analyzed the role of mediators in the Leishmania-host interaction in the experimental and clinical context, aiming to identify the main cell types studied, as well as the main eicosanoids and their influence during the infection. The main lipid mediators studied were the eicosanoids LTB₄ and PGE₂, which are related to the inflammatory response in cutaneous and visceral leishmaniasis. In vitro models using macrophages and neutrophils infection reveal that LTB₄ plays a fundamental role in reducing the parasite load, while PGE₂ and PGF_2α suppress the immune response, favoring the survival of the parasite in the host. In the in vivo infection, PGE₂ is related to the visceralization process of the disease and the persistence of tegumentary lesions. An emerging role in pathophysiology has been pointed out for the mediators of the HETE class and for Resolvin D₁, which act favoring Leishmania infection and are associated with more severe cases of the disease. Thus, it can be concluded that lipid mediators play crucial roles in the Leishmania-host interaction, modulating the inflammatory response and disease progression. Studies exploring the contribution of intervention in the production of lipid mediators during the course of the disease are still needed.