Role of macrophage inflammatory protein-1alpha (MIP-1alpha) in macrophage homing in the spleen and heart pathology during experimental infection with Trypanosoma cruzi.

We investigated in vivo the effect of macrophage inflammatory protein-1alpha (MIP-1alpha) inhibition upon the cellular recruitment into tissue damage sites and spleen histology in mice acutely infected with Trypanosoma cruzi. Histopathological studies of spleen sections revealed a 68% decrease in macrophage/monocyte infiltration as a result of MIP-1alpha neutralisation. Moreover, a reduction in the number of plasma cells and immunoblasts was observed. However, antibody (Ab)-mediated blocking of MIP-1alpha failed to modify tissue parasite levels. Examination of myocardial sections showed an increase in inflammatory lesions in mice treated with anti-MIP-1alpha Ab. There was also an increasing trend in the number of amastigote nests in the myocardium of anti-MIP-1alpha-treated mice compared with controls. Administration of anti-MIP-1alpha Ab failed to affect either the extent of inflammatory infiltrates or the parasite count in liver and skeletal muscle. To the best of our knowledge, these data are the first in vivo demonstration that Cz.sbnd;C chemokine MIP-1alpha is involved in cellular recruitment during acute infection with T. cruzi, indicating that MIP-1alpha influences macrophage/monocyte influx into target organs.