Investigation of the expressions of some inflammatory and complement pathway genes at the mRNA and protein level in gerbils infected with Leishmania major

Leishmaniasis caused by Leishmania species, one of the intracellular protozoa, is a systemic, chronic disease that causes skin and internal organ infections and its prevalence has increased in recent years. The immunity mechanisms created by the immune system against Leishmania species, which are important for public health and can infect immune system cells, have not been completely revealed. For this purpose, in this study, it was aimed to create a L. major infection model in gerbils (Meriones unguiculatus), investigate of the expression levels of IL-1β, IL-2, IL-6, IFN-ɣ, TNF-α genes and their roles in the inflammatory response in order to determine the response of immune system cells against Leishmania infections, determining the expression levels of MBL-1, MBL-2, C2, C3 genes to examine the role of the lectin pathway in the complement system, and the protein expression levels of MBL-1, C2, C3 from these genes, performing biochemical tests (GSH and MDA) to detect oxidative stress that may occur against infection in gerbils and finally hematological analyzes to evaluate the leukocyte counts in the blood. In this connection, the cutaneous leishmaniasis animal model was created in gerbils firstly, and the presence of parasites was determined in the samples obtained from the lesion areas by microscopic examinations and culture studies. It was determined that the expression levels of inflammatory cytokine and complement system genes increased significantly in infected gerbils, oxidative stress occurred due to decreased GSH and increased MDA levels, and the amount of leukocytes increased significantly due to the infection. At the end of the study, Th1, Th2, and complement system pathways were determined to be activated in the cutaneous leishmanisis, infections, and it was reached the conclusion that different immunopathological mechanisms should also be evaluated in the pathogenesis of the disease.