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Sequential Changes of the Connective Matrix Components of the Myocardium (Fibronectin and Laminin) and Evolution of Cardiac Fibrosis in Mice Infected with Trypanosoma cruzi

Interstitial matrix alterations due to chronic Trypanosoma cruzi myocarditis were studied in mice by immunofluorescent microscopy with specific purified antibodies against the main different collagen isotypes, laminin and fibronectin. During the early subacute stage (26–30 days postinfection), sarcolemmal and perivascular deposits of laminin and fibronectin were prominent. The presence of fibronectin appeared to correlate with the presence of inflammatory cells. By the late subacute phase and early chronic phase (50–90 and 80–90 days postinfection, respectively), laminin and Type IV collagen were present. These were the principal features, although fibronectin continued to be found among inflammatory cells, and pro-III and III collagens formed irregular bands and periarteriolar deposits. During the late chronic phase (150–200 days postinoculation) the interstitium was enlarged and irregular, with positive staining for laminin, Types III, pro-III, and IV collagens; fibronectin appeared as focal, subendocardial, interstitial, and perivascular deposits.

The relative absence of Type I collagen and the apparent positive correlation between interstitial matrix amplification and the presence of mononuclear inflammatory cells suggest that fibrotic changes in chronic T. cruzi myocarditis can be reversed if the inflammatory changes subside.