Characterization of enteroglial cells and denervation process in chagasic patients with and without megaesophagus

Summary 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...

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Veröffentlicht in:Human pathology 2010-04, Vol.41 (4), p.528-534
Hauptverfasser: Nascimento, Rodolfo Duarte, de Souza Lisboa, André, Fujiwara, Ricardo Toshio, de Freitas, Michelle Aparecida Ribeiro, Adad, Sheila Jorge, Oliveira, Rodrigo Correa, d'Ávila Reis, Débora, da Silveira, Alexandre Barcelos Morais, PhD
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Sprache:eng
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Zusammenfassung:Summary 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.
ISSN:0046-8177
1532-8392
DOI:10.1016/j.humpath.2009.05.018