ABSTRACT
Chagas' disease is one of the most serious parasitic diseases of Latin America, with a social and economic impact far outweighing the combined effects of other parasitic diseases such as malaria, leishmaniasis and schistosomiasis. In the chronic phase of this disease, the destruction of enteric nervous system (ENS) components leads to megacolon development. Previous data presented that the regeneration tax in the ENS neurons is augmented in chagasic patients. Although, there are several neuronal types with different functions in the intestine a detailed study about the regeneration of every neuronal type was never performed before. Therefore, the aim of this study was to evaluate the regeneration tax of every neuronal cell type in the ENS from chagasic patients with megacolon and non-infected individuals. A neuronal regeneration marker (GAP-43) was used in combination with a pan-neuronal marker (Peripherin) and several neuropeptides markers (cChat, Substance P, NPY, VIP and NOS), and it was considered as positive just with the combination of these markers. Our results demonstrated that the regeneration levels of cChat, Substance P, and NPY were similar in chagasic patients and non-infected individuals. However, levels of VIP and NOS neuropeptides were increased in chagasic patients when compared with non-infected individuals. We believe that the augment in the regeneration occur due to an increased destruction of selective neuronal types. These results corroborates with previous studies that pointed out to selective destruction of VIP and NOS neurons in chagasic patients.
Subject(s)
Chagas Disease/metabolism , Chagas Disease/pathology , Megacolon/pathology , Neurons/metabolism , Regeneration , Adult , Aged , Enteric Nervous System/metabolism , Female , GAP-43 Protein/metabolism , Ganglia, Autonomic/metabolism , Humans , Male , Middle Aged , Nitric Oxide Synthase/metabolism , Vasoactive Intestinal Peptide/metabolismABSTRACT
Chagas disease is caused by infestation with the parasite Trypanosoma cruzi, and some patients who are serologically positive develop chronic megaesophagus, whereas others are symptom-free. Gastrointestinal form of Chagas disease involves an inflammatory invasion of the enteric plexuses and degeneration of enteric neurons and previous works related that enteroglial cells would be involved in enteric inflammatory responses. Because of this, the aims of this study were to determine the relation of enteroglial cells with the denervation process in chagasic patients with and without megaesophagus and seronegative individuals. Our results indicated that the innervation of the esophageal muscle was substantially reduced in patients with megaesophagus, but asymptomatic seropositive subjects were not different to seronegative controls. Besides, patients with megaesophagus had significant decreased of enteroglial cells labeled with S-100 and glial fibrillary acidic protein, whereas patients without megaesophagus presented an increased of both labels. We believe that enteroglial cells would operate a mechanism of defense in the enteric nervous system against the Trypanosoma cruzi infection, which could prevent the organ denervation and preserve the esophagus function.
