1999 Abstract: 2098 CELL MEDIATED IMMUNE RESPONSE IN MEGACOLON FROM PATIENTS WITH CHRONIC CHAGAS' DISEASE
Abstracts 1999 Digestive Disease Week
# 2098
CELL MEDIATED IMMUNE RESPONSE IN MEGACOLON FROM PATIENTS WITH CHRONIC CHAGAS' DISEASE
Ulysses Ribiero, M Okumura, A Habr-Gama, J J Gama-Rodrigues, C E P Corbett, Univ of Sao Paulo, Sao Paulo Brazil
The mechanism of lesion of the myenteric and submucosal plexus of the bowel in patients with megacolon due to Chagas' disease is incompletely understood. It has been shown the parasitism of the neuronal cells and mononuclear inflammatory cells near the autonomic plexus during the acute phase of the disease. Aim: To evaluate the role of inflammatory cells and the subclasses of lymphocytes involved in the neuropathic lesions in the colon of patients who underwent resections for advanced megacolon and to compare with controls. Methods: Specimens from 23 patients were selected based on histopathological analysis with hematoxylin-eosin. Paraffin-embedded tissue blocks were sectioned and evaluated by immunohistochemistry for T. cruzi, CD3, CD8 and NK.1 antibodies using avidin-biotin peroxidase method. Results: Almost every myenteric plexuses were damaged, characterized by degenerative changes, necrosis of ganglion cells and inflammatory response. Mild lymphocytic infiltration around degenerative and/or normal ganglion cells was observed in all cases. Some ganglion cells were surrounded by collagen fibers and mononuclear cells. Immunohistochemistry for T. cruzi stained the nucleus and cytoplasm of ganglion cells, and the inflammatory cells. Most of the inflammatory cells were lymphocytes, classified as CD3 positive cells. CD8 was expressed in a small number of the lymphocytes and was associated to degenerated ganglion cells. NK.1 was detected in a lower proportion and was distributed between the muscle layers or in proximity to the plexus. All these findings were observed in lesser degree in the submucosal plexus. Conclusion:The pathogenesis of the chronic megacolon is based on continuous process of ganglion cell damage with participation of lymphocytes, expressing CD8 and NK.1 membrane antigens and probably parasite antigen.