Cell-mediated immune response in megacolon from patients with chronic Chagas' disease

PURPOSE: The mechanisms that control chronic infection in vivo and the immu nologic mechanisms involved in the pathogenesis of chagasic megacolon are n ot completed characterized. Although autoimmunity may play a role in the pa thogenesis of Chagas' disease, recent studies, both in mice and in humans, suggest a positive association of tissue parasitism, inflammation, and seve rity of lesions. The aim of this study was to evaluate the role of inflamma tory cells and the subclasses of lymphocytes involved in neuropathic lesion s in the colon of patients who underwent resection for advanced megacolon. METHODS: Specimens from 23 patients were selected based on histopathologic analysis. Paraffin-embedded tissue blocks were sectioned and evaluated by i mmunohistochemistry for cluster of differentiation 3, cluster of differenti ation 8, cluster of differentiation 20, and natural killer cell antibodies by an avidin-biotin peroxidase method. RESULTS: Almost all myenteric plexus es were damaged, characterized by degenerative changes, necrosis of ganglio n cells, and inflammatory response. Mild lymphocytic infiltration around de generated and normal ganglion cells was observed in all cases. Collagen fib ers and mononuclear cells surrounded some ganglion cells. Most of the infla mmatory cells were lymphocytes, identified as cluster of differentiation 3- positive cells. Cluster of differentiation 8-positive lymphocytes were asso ciated with degenerated ganglion cells. Natural killer cell antibodies were detected in a lower proportion of cells and were distributed between muscl e layers or in proximity to the myenteric plexus. AU these findings were al so observed in the submucosal plexus. Cluster of differentiation 20-positiv e lymphocytes were not present in muscle layers or in the vicinity of eithe r plexus. CONCLUSION: Pathogenesis of the megacolon is based on a continuou s process of ganglion cell damage with participation of T lymphocytes expre ssing cluster of differentiation 8 and natural killer cell membrane antigen s. B lymphocytes do not take parr in the chronic inflammatory reaction.