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5-HT3A serotonin receptor in the gastrointestinal tract: the link between immune system and enteric nervous system in the digestive form of Chagas disease

  • Immunology and Host-Parasite Interactions - Short Communication
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Abstract

Chagas disease is caused by Trypanosoma cruzi and remains one of the most neglected diseases in Latin America. One of its clinical forms is Chagas megacolon. Despite being known for more than half a century, detailed causes are still obscure. Recent evidence indicates a close relationship between the immune system and the enteric nervous system in the etiology of chagasic megacolon pathology. It is believed that low expression of the 5-HT3A serotonin receptor on lymphocytes could be linked to megacolon development. To test this hypothesis, this work investigated the distribution of CD4, CD8, and CD20 lymphocytes and their 5-HT3A receptor expression. The results demonstrated that Chagas patients without megacolon present a higher expression of the 5-HT3A receptor in all analyzed lymphocytes compared with Chagas patients with megacolon. These data suggest that the high expression of this receptor may lead to immunomodulation and prevent the development of Chagas megacolon.

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Funding

This work was supported by funds from CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico) Grant 404718/2016-7, Brazil.

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Correspondence to Alexandre Barcelos Morais da Silveira.

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Informed consent was obtained from the patient or family members prior to tissue procurement, and this work was approved by Universidade Federal de Uberlândia Research Ethics Committee (ETIC no 110/11) according to Guidelines and Norms for Research Involving Human Beings, Resolution CNS 466/2012, Brazil.

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Section Editor: Sarah Hendrickx

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de Oliveira, J.A., Freitas, M.A.R., de Oliveira, E.C. et al. 5-HT3A serotonin receptor in the gastrointestinal tract: the link between immune system and enteric nervous system in the digestive form of Chagas disease. Parasitol Res 118, 1325–1329 (2019). https://doi.org/10.1007/s00436-019-06241-w

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  • DOI: https://doi.org/10.1007/s00436-019-06241-w

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