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Cardiomyopathy is the most serious consequence of Chagas disease, a neglected human disorder caused by  Trypanosoma cruzi  infection. Because  T .  cruzi  parasites invade cardiomyocytes, we sought to investigate whether these cells recognize the parasite  in vivo  by receptors signaling through the MyD88 adaptor, which mediates the activation pathway of most Toll-like receptors (TLRs) and IL-1/IL-18 receptors, and influence the development of acute cardiac pathology. First, we showed that HL-1 cardiac muscle cell line expresses MyD88 gene and protein at resting state and after  T .  cruzi  infection. To evaluate the role  in vivo  of MyD88 expression in cardiomyocytes, we generated Mer + MyD88flox +/+  mice in which tamoxifen treatment is expected to eliminate the  MyD88  gene exclusively in cardiomyocytes. This Cre-loxP model was validated by both PCR and western blot analysis; tamoxifen treatment of Mer + MyD88flox +/+  mice resulted in decreased MyD88 gene and protein expression in the heart, but not in the spleen, while had no effect on littermates. The elimination of MyD88 in cardiomyocytes determined a lower increase in  CCL5 ,  IFNγ  and  TNFα  gene transcription during acute infection by  T .  cruzi  parasites of the Y strain, but it did not significantly modify heart leukocyte infiltration and parasitism. Together, our results show that cardiomyocytes can sense  T .  cruzi  infection through MyD88-mediated molecular pathways and contribute to the local immune response to the parasite. The strong pro-inflammatory response of heart-recruited leukocytes may overshadow the effects of MyD88 deficiency in cardiomyocytes on the local leukocyte recruitment and  T .  cruzi  control during acute infection.

plos neglected tropical diseases

MyD88 activation in cardiomyocytes contributes to the heart immune response to acute Trypanosoma cruzi infection with no effect on local parasite control