Oral dependent-dose toxoplasmic infection model induced by oocysts in rats: Myenteric plexus and jejunal wall changes

Abstract

Toxoplasmosis is a widely distributed disease caused by the protozoan Toxoplasma gondii that is mainly transmitted orally. Once ingested, the parasite crosses the intestinal barrier to reach the blood and lymph systems to migrate to other regions of the host. The objective of this study was to evaluate the changes in the myenteric plexus and the jejunal wall of Wistar rats caused by oral infection with T. gondii oocysts (ME-49 strain). Inocula of 10, 100, 500 and 5000 oocysts were used. The total population of myenteric neurons and the most metabolically active subpopulation (NADH-diaphorase positive - NADH-dp) exhibited a decrease proportional to the dose of T. gondii. There was also a quantitative increase in the subpopulation of NADPH-diaphorase-positive (NADPH-dp) myenteric neurons, indicating greater expression of the NOS enzyme. Neuronal atrophy was observed, and morphological and morphometric alterations such as jejunal atrophy were found in the infected groups. Hypertrophy of the external muscle with the presence of inflammatory foci was observed in the group infected with 5000 oocysts. The changes observed in the infected groups were proportional to the number of oocysts inoculated.

Toxoplasma gondii promotes changes in VIPergic submucosal neurons, mucosal intraepithelial lymphocytes, and goblet cells during acute infection in the ileum of rats

“…This increase may represent a protective mechanism, as nNOS is involved in maintaining the integrity of the mucosa (epithelial barrier) and epithelial secretion in the gastrointestinal tract . Our data are in accordance with other studies in the myenteric plexus of the jejunum of rats in the chronic phase of toxoplasmosis . This increase does not necessarily represent cell proliferation, but rather a change in phenotype …”

“…Toxoplasma gondii oocysts of the ME‐49 strain, genotype II, were used. The animals of infected groups received 1.0 ml of oral suspension containing 5000 sporulated T. gondii oocysts . The CG received the same volume of sterile saline solution.…”

Different inoculum loads of Toxoplasma gondii induce reduction of myenteric neurons of the rat colon

“…This phenomenon may indicate a relationship between the immune response against the parasite and the production of nitric oxide in the myenteric plexus. This is corroborated by similar studies of the jejunum of these animals (VICENTINO-VIEIRA et al, 2015) and that of pigs (ODORIZZI et al, 2010), in which a genotype III strain was used. However, no studies were found about the effects of toxoplasmosis infection on the NADPH-d + neurons specific to the colon.…”

“…This divergence in findings is explained by differences in the experimental protocol, such as the evolutionary form of the inoculated parasite and the genotype of the strain. A study of the small intestine in which a similar experimental protocol was used revealed neuronal loss with inoculum loads of 10, 100, 500 and 5000 oocysts, demonstrating a greater depletion effect of the infection on neurons in the initial part of the intestines (VICENTINO-VIEIRA et al, 2015). This can be explained by the natural presence of a larger number of intraepithelial lymphocytes in the small intestine, resulting in a more intense immune response with greater release of cytokines and other inflammatory mediators, and hence, greater tissue damage (BEAGLEY et al, 1995).…”

Acute Toxoplasma gondii infection alters the number of neurons and the proportion of enteric glial cells in the duodenum in Wistar rats

“…We have shown that the infection can compromise the intestinal structure and innervation, even in immunocompetent individuals with no classic clinical signs of toxoplasmosis . We observed local inflammation that was possibly induced by the presence of the parasite in the organ, reflected by the presence of tissue cysts and parasitic DNA . The submucosal plexus and EGCs appear to play a primordial role in the response to infection .…”