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Toxoplasma gondii infection impairs the colonic motility of rats due to loss of myenteric neurons
Author(s) -
Machado Camila Cristina Alves,
Watanabe Paulo da Silva,
Mendes Joana D’Arc de Lima,
Pupim Andréia Carla Eugenio,
Ortigoza Silvia Miyazaki,
Bergoc Heloisa Gonçalves,
Nino Beatriz de Souza Lima,
Góis Marcelo Biondaro,
Garcia João Luis,
Blackshaw L. Ashley,
Sant´Ana Débora de Mello Gonçales,
Araújo Eduardo José de Almeida
Publication year - 2021
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.13967
Subject(s) - myenteric plexus , motility , toxoplasma gondii , cholinergic neuron , biology , diarrhea , cholinergic , medicine , gastroenterology , enteric nervous system , feces , pathology , immunology , immunohistochemistry , antibody , genetics , paleontology
Abstract Background Toxoplasma gondii infection causes intestinal inflammation and diarrhea indicating possible intestinal motor dysfunction. Anatomical studies have shown alterations in the colonic myenteric plexus, but it is unknown whether this impacts motility and therefore whether motility is a target for treatment. We determined whether colonic coordinated movements are compromised by toxoplasmic infection and how it is associated with anatomical changes. Methods Male Wistar rats were evaluated at 6, 12, 24, 48, and 72 hours and 30 days postinfection (dpi) and controls. Infected rats received orally 5 × 10 3 sporulated oocysts of strain ME‐49 (genotype II) of T gondii . The colon was collected for anatomical analysis (including the myenteric plexus immunolabeled with HuC/D, nNOS, and ChAT) and motility analysis in vitro (conventional manometry). Fecal output was measured daily. Key Results At 12 hours postinfection, T gondii caused hypertrophy of the muscularis externa layer of the distal colon. There was loss of total, nitrergic, and cholinergic myenteric neurons in the proximal colon at 30 day postinfection (dpi); however, only loss of cholinergic neurons was found in the distal colon. Contractile complexes in the middle and distal colon were longer in duration in infected animals, which was associated with slower migration of the colonic motor complex. However, gastrointestinal transit time and fecal pellet output remained unchanged during the T gondii infection. Conclusions and Inferences Toxoplasma gondii caused myenteric neuronal loss in the proximal and distal colon and altered the motility pattern in the middle and distal colon to a more propulsive phenotype.