CCL3/Macrophage Inflammatory Protein-1α Is Dually Involved in Parasite Persistence and Induction of a TNF- and IFNγ-Enriched Inflammatory Milieu in Trypanosoma cruzi-Induced Chronic Cardiomyopathy.
CCL3, member of the CC-chemokine family, has been linked to heart tissue macrophage recruitment and parasite control in mouse acute infection with Trypanosoma cruzi, the causative agent of Chagas disease. Here, we approached CCL3 participation in chronic chagasic cardiomyopathy (CCC), the main clinical forms of Chagas disease . We CCC Rat Recombinant Proteins induced in C57BL / 6 (ccl3 + / +) and CCL3-deficiency (ccl3 - / -) mice by infection with Colombia Type I strain. In ccl3 + / + mice, high levels CCL3 mRNA and protein were detected in heart tissue during acute and chronic infections. Survival is not affected by the shortage CCL3. Compared with ccl3 + / +, ccl3 chronically infected - / - mice presented decreased cardiac parasitism and inflammation caused by CD8 + cells and macrophages. Leukocytosis decreased in infected ccl3 - / - mice, in line with the accumulation of CD8 + T cells with no CCR5 + activated LFA-1 + cells in the spleen. Furthermore, T. cruzi-infect...