MMGL receptor plays an important role to macrophage activation during Trypanosoma cruzi infection

Abstract

Abstract The C-type lectin receptor (MGL) is exclusively expressed on macrophages (MΦs) and dendritic cells (DCs), recognizes glycosylated antigens, particularly galactose (Gal) and N-acetylgalactosamine (GalNAc), that are present in tumors, fungi and viruses. However, little is known the role of MGL in the interaction with parasites. We evaluated the role of murine MGL (mMGL) in the activation and functionality of MΦs in Trypanosoma cruzi (T. cruzi) infection, a parasite that has molecules glycosylated rich in Gal and GalNAc in its membrane. Peritoneal MΦs from C57BL/6 WT and mMGL nockout (mMGL−/−) mice were infected in vitro with epimastigotes of T. cruz,i Qro strain (10000 parasites). The percentage of infected MΦs and the number of internalized parasites/MΦs was analyzed by microcopy. Cytokines TNF-α, IL-12 and IL-10 were determine in supernatants by ELISA. The trypanocidal capacity of MΦs was determined by the incorporation of tritiated thymidine ([3H] TdR). Expression of TLR-4, TLR-2 and mannose receptor (MR) in MΦs stimulated in vitro with T. cruzi antigen was analyzed by flow cytometry. mMGL−/− MΦs were higher infected with more parasites per MΦ and had a reduced capacity to eliminate the T. cruzi, these were associated to lower levels of TNF-α, TLR-4 and MR expression compared to WT MΦs. These results demonstrate that absence of mMGL favors susceptibility to infection with T. cruzi, suggesting a regulatory role of mMGL on the expression of other important receptors in the immune response to T. cruzi infection.