ABSTRACT
Cutaneous leishmaniasis is the most common form of leishmaniasis in humans, factors such as poverty, poor housing, inadequate domestic hygiene, malnutrition, mobility, and occupational exposure are risk factors associated with the condition, however, there are few studies focused on determining the immune mechanism involved in the resolution of cutaneous leishmaniasis caused by the species Leishmania mexicana, as well as possible environmental factors such as solar radiation, which could contribute to its establishment. through mechanisms immunosuppressants, of which to date is unknown. In this study, the effect of UV-B light was evaluated as a risk factor affecting components of the innate immune response 3 days after infection with L. mexicana. A delayed-type hypersensitivity reaction (DTH) was used to evaluate immunosuppression induced by UV-B light. Through a histological analysis, the skin lesions of the mice (Hematoxylin & Eosin) were evaluated, the presence of mast cells and their level of degranulation (toluidine blue staining), the presence of IL-10+ and MOMA2+ cells were analyzed by immunohistochemistry and finally, the cytokine profile was evaluated by qPCR in the skin lesions tissue. An alteration in the architecture of the tissue was observed, as well as a greater number of mast cells, both complete and degranulated, as well as an increase in IL-10+ and MOMA2+ cells in the skin lesions of the mice that were irradiated and subsequently infected, when compared with the lesions of infected mice (P> 0.0001), immunomodulation was also observed in the profile of cytokines expressed between both groups analyzed. This is the first study to demonstrate the effects of UV-B radiation on components of the innate immune response at short times of infection by L. mexicana.
