Peripheral blood monocytes show morphological pattern of activation and decreased nitric oxide production during acute Chagas' disease in rats.

Peripheral blood monocytes (PBM) recruitment is a rapid and remarkable phenomenon during acute infection with the intracellular protozoan parasite Trypanosoma cruzi, the causative agent of Chagas' disease. The functional capabilities of these cells during the infection, however, are poorly understood. The purpose of the present study was to determine whether PBM are morphologically activated and produce nitric oxide (NO), a mediator of host cell defense when challenged with the parasite at different time points of acute disease. In parallel, the parasite load was monitored in the blood and heart, a target organ of the disease, as well as the PBM numbers. The infection did not induce NO release by PBM, although these cells exhibited a clear morphological pattern of activation characterized by irregular surface, increase of organelle amount, especially Golgi complex, and cell size. On the contrary, there was significant inhibition of NO production by PBM at the beginning (day 6) and end of acute disease (day 20). At this time, the levels of NO were inversely related to the arginase activity, an enzyme that affects the NO synthesis. The mobilization process of PBM occurred in parallel to parasite load and was associated with the resolution mechanism of parasitemia and heart parasitism. Our results showed that activated PBM are notably involved in the host response to the acute T. cruzi infection in rats. However, the in vivo NO production by these cells seems to be inhibited during the acute Chagas' disease through a mechanism involving the arginase pathway.