Increased expression and secretion of ICAM‐1 during experimental infection with Trypanosoma cruzi

Abstract

In the present study we demonstrate that spleens and hearts from BALB/c mice infected with the virulent Tulahuén or the low virulent CA-I strains of Trypanosoma cruzi, contain substantially higher ICAM-1 transcripts than uninfected controls. ICAM-1 expression in heart cells was also increased in the protein level, as measured by flow cytometry, ELISA and immunohistochemistry. The adhesive receptor was observed not only on inflammatory cells but also on sarcolemma of cardiac myocytes from T. cruzi infected mice. ICAM-1 expression was higher during the acute phase than in the chronic phase of infection, and paralleled the density of inflammatory leukocytes. Elevated titres of soluble ICAM-1 (s-ICAM-1) were detected in sera from mice during the acute phase of infection with CA-I or Tulahuén parasites. Cytokines, including IFN-gamma, IL-1 alpha, IL-6 and TNF-alpha have been shown to modulate expression of ICAM-1. Spleens and hearts from mice infected with CA-I or Tulahuen strains showed increased accumulation of mRNAs specific for these cytokines, which peaked during the acute phase of infection. However, IFN-gamma activity was not necessary for ICAM-1 induction, as its levels were also increased during infection in IFN-gamma receptor knock-out (IFN-gamma R- ) mice. Upregulation of ICAM-1 expression might be a direct consequence of parasite infection, since its density on cell lines of different lineages was enhanced after 24 or 48 h of infection with T. cruzi.

Cellular and Cytokine Characterization of Vascular Inflammation in CBA/J Mice Chronically Infected with Trypanosoma cruzi

“…In both the acute and the chronic stages, the myocytes within the heart were ICAM-1 positive. This finding is in agreement with our previous data of ICAM-1 expression at both protein and RNA levels using other mouse and parasite strains [18].…”

Differential expression of adhesion moleculesshaping the T-cell subset prevalence during the early phase of autoimmune and Trypanosoma cruzi-elicited myocarditis

“…In agreement with our results, previous report has shown that LFA-1 + mononuclear cells are present in the inflamed myocardium of chronic chagasic patients with severe cardiomyopathy (Reis et al 1993), suggesting that at least part of these inflammatory cells are activated. Further, we bring evidence that the myocytes present enhanced ICAM-1 expression, confirming a previous report (Laucella et al 1996). Furthermore, as LFA-1/ICAM-1 interactions play a crucial role forming the immunological synapse (Camacho et al 2001), ICAM-1 + myocytes could be targets for LFA-1 + cytotoxic T-cells, contributing to heart dysfunction.…”

Intercellular Adhesion Molecule 1 Deficiency Leads to Impaired Recruitment of T Lymphocytes and Enhanced Host Susceptibility to Infection withTrypanosoma cruzi

“…Moreover, ICAM-1 ϩ and VCAM-1 ϩ blood vessels were associated with the presence of CD8 ϩ -infiltrating T cells in the cardiac tissue of chagasic patients with severe cardiomyopathy (38). In addition, cardiomyocytes express ICAM-1 during the acute phase of experimental T. cruzi infection (27,30). Considering that ICAM-1-mediated interactions plays a crucial role in forming the immunological synapse (29,39), ICAM-1 ϩ myocytes could be targets for LFA-1 ϩ cytotoxic T cells, contributing to heart dysfunction during chagasic myocarditis.…”

“…The PCR products were separated by acrylamide gel electrophoresis and stained with silver nitrate. The primers sequences and PCR product sizes have bee n published elsewhere (30).…”