alexa Nitrergic Myenteric Neurons are Spared in Experimental Chagasic Megacolon
E-ISSN: 2314-7326
P-ISSN: 2314-7334

Journal of Neuroinfectious Diseases
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Research Article

Nitrergic Myenteric Neurons are Spared in Experimental Chagasic Megacolon

Mayra Fernanda Ricci1, Camila França Campos1, Christiane Teixeira Cartelle1, Samantha Ribeiro Béla1, Silvia Dantas Cangussú2, Helton da Costa Santiago3, Camila Megale de Almeida-Leite4 and Rosa Maria Esteves Arantes1*

1Department of Pathology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil

2Departament of Biological Sciences ̸LAFEX, Federal University of Ouro Preto, Ouro Preto, Minas Gerais, Brazil

3Departament of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil

4Departament of Morphology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil

*Corresponding Author:
Rosa Maria Esteves Arantes
Department of Pathology, Institute of Biological Sciences
Federal University of Minas Gerais
Av. Antonio Carlos, 6627, Pampulha
Belo Horizonte, Minas Gerais, Brazil
Tel: 3134092896
Fax: 31 3409-2879
E-mail: [email protected]

Received date: November 23, 2016; Accepted date: December 21, 2016; Published date: December 23, 2016

Citation: Ricci MF, Campos CF, Cartelle CT, Béla SR, Cangussú SD, et al. (2016) Nitrergic Myenteric Neurons are Spared in Experimental Chagasic Megacolon. J Neuroinfect Dis 7:235. doi:10.4172/2314-7326.1000235

Copyright: © 2016 Ricci MF, et al. This is an open-access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Chagas disease is a chronic disorder caused by the Trypanosoma cruzi protozoan. The infection causes alterations to the enteric nervous system such as megaesophagus and megacolon. There is evidence of denervation of myenteric ganglia. The intense parasitism of acute phase affects neuronal integrity but contrasts with the absence of parasites and the discreet inflammatory process of chronic phase, indicating a progressive injury mechanism that needs to be better understood in the megacolons. The potential selectivity of enteric neurons classes affected by the progression of the disease is not yet clear. Nitrergic neurons which co-localize other neurotransmitters represent the most common inhibitory neuron of the ENS. Recently a chronic stage of the Chagas disease was reproduced experimentally in a suitable murine model of megacolon. Considering the limitation of studying human intestine and the controversy on the pattern of nNOS involvement in chagasic megacolon, we decided to assess the nitrergic neurons in the myenteric plexus of mice. We used antibodies against structural protein gene product 9.5 (PGP 9.5) and functional neuronal nitric oxide synthase (n-NOS) at the acute and chronic phase of the disease to quantify myenteric ganglionar neurons in the colon of infected and non-infected mice. We found a reduction in the ganglionar number of neurons detected by anti-protein gene product 9.5 antibodies in colon from mice at the chronic stage. However, the number of nitrergic neurons per ganglia remained unchanged along the acute to phase chronic of the disease. Our findings indicate a long-term preservation of nitregic neurons detrimental to other classes of enteric in our model of experimental Chagas disease. We propose that differential loss of enteric neurons is at least one of the structural substrate for the development of the longterm morphfunctional changes that lead to the megacolon.

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