INCREASED EXPRESSION AND SECRETION OF ICAM-1 DURING EXPERIMENTAL-INFECTION WITH TRYPANOSOMA-CRUZI

In the present study we demonstrate that spleens and hearts from BALB/ c mice infected with the virulent Tulahuen or the low virulent CA-I st rains of Trypanosoma cruzi, contain substantially higher ICAM-1 transc ripts than uninfected controls. ICAM-1 expression in heart cells was a lso increased at the protein level, as measured by flow cytometry, ELI SA and immunohistochemistry. The adhesive receptor was observed not on ly on inflammatory cells but also on sarcolemma of cardiac myocytes fr om T. cruzi infected mice. ICAM-1 expression was higher during the acu te phase than in the chronic phase of infection, and paralleled the de nsity of inflammatory leukocytes. Elevated titres of soluble ICAM-1 (s -ICAM-1) were detected in sera from mice during the acute phase of inf ection with CA-I or Tulahuen parasites. Cytokines, including IFN-gamma , IL-1 alpha, IL-6 and TNA-alpha have been shown to modulate expressio n of ICAM-1. Spleens and hearts from mice infected with CA-1 or Tulahu en strains showed increased accumulation of mRNAs specific for these c ytokines, which peaked during the acute phase of infection. However, I FN-gamma activity was not necessary for ICAM-1 in IFN-gamma receptor k nock-out (IFN-gamma R(-)) mice. Upregulation of ICAM-1 expression migh t be a direct consequence of parasite infection, since its density on cell lines of different lineages was enhanced after 24 or 48 h of infe ction with T. cruzi.