Myenteric neuroprotective role of aspirin in acute and chronic experimental infections with Trypanosoma cruzi.

Abstract

Experimental and clinical studies have shown that myenteric neuron cell death during infection with Trypanosoma cruzi mainly occurs in the esophagus and colon, resulting in megaesophagus and megacolon, respectively. Evidence suggests that the cyclooxygenase enzyme (COX) is involved in the T.cruzi invasion process. The use of low-dose aspirin (ASA), a COX-1/COX-2 inhibitor, has been shown to reduce infection with T.cruzi. Therefore, in this study, we evaluated the effects of treatment with low-dose ASA on myenteric colonic neurons during murine infection with T.cruzi. Swiss mice were assigned into groups treated with either phosphate-buffered saline or low doses of ASA during the acute phase (20mg/kg ASA) and chronic phase (50mg/kg ASA) of infection with the Y strain of T.cruzi. Seventy-five days after infection, colon samples were collected to quantify inflammatory foci in histological sections and also general (myosin-V+ ), nitrergic, and VIPergic myenteric neurons in whole mounts. Gastrointestinal transit time was also measured. Aspirin treatment during the acute phase of infection reduced parasitemia (P<.05). Aspirin treatment during the acute or chronic phase of the infection reduced the intensity of inflammatory foci in the colon, protected myenteric neurons from cell death and plastic changes, and recovered the gastrointestinal transit of mice infected with T.cruzi (P<.05). Early and delayed treatment with low-dose ASA can reduce the morphofunctional damage of colonic myenteric neurons caused by murine T.cruzi infection.