Hypertrophy of NADH-diaphorase positive myenteric neurons in rat jejunum after acute infection caused by Toxoplasma gondii

Ls, Pereira; Silva, AV; Araújo, Eja; Sant'Ana, Dmg

doi:10.1590/s1678-91992010000200011

Cited by 10 publications

(5 citation statements)

References 28 publications

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“…The maintenance of the area of the gut was similar to what was seen in previous studies involving toxoplasmic infection in rats (Soares et al, 2009;Sugauara et al, 2009;Pereira et al, 2010). These findings indicate that the toxoplasmic infection caused by the strain used in this study may not have changed the structure of the intestinal wall; however, we suggest that morphometric studies evaluating the strata of the jejunal wall are needed to verify this hypothesis.…”

Section: Discussionsupporting

confidence: 90%

“…Cell bodies of enteric neurons are organised in the submucosal and myenteric plexus (Furness, 2006). Recent studies showed that infection with T. gondii causes morphometric changes in the myenteric neurons of rats (Sugauara, et al, 2008(Sugauara, et al, , 2009Soares et al, 2009;Pereira et al, 2010) and pigs (Odorizzi et al, 2010). However, the total population and the NADPH-diaphorase positive myenteric neurons were evaluated by these studies, and there are no studies involving the two most prevalent subpopulations of myenteric neurons: nitrergic and cholinergic (Phillips et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…The sporozoites are located within the oocysts, which remain free in the environment and therefore represent the most common infectious form (Dubey et al, 1998;Tenter, 2009). The only study evaluating the infection caused by oral inoculation with oocysts in rats analysed the subpopulation of NADH-dp myenteric neurons (Pereira et al, 2010). In other preliminary studies on rodents, the effects of the infection caused by tachyzoites (Sugauara et al, 2008;Soares, et al, 2009) and bradyzoites (Sugauara et al, 2009) were evaluated without analysing the infection with oocysts from this parasite.…”

Section: Introductionmentioning

confidence: 99%

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Chronic infection with Toxoplasma gondii causes myenteric neuroplasticity of the jejunum in rats

Hermes-Uliana

Pereira-Severi

Luerdes

et al. 2011

Autonomic Neuroscience

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Toxoplasma gondii is an aetiological agent of toxoplasmosis, which commonly causes diarrhoea in a number of species. This observation and the parasite's affinity for the nervous tissue support the theory that T. gondii infection may affect the myenteric neurons. The aim of this study was to evaluate the changes caused by T. gondii (genotype III) in the myenteric neurons of the jejunum in rats. Fifteen rats were distributed into three groups: control (CG), inoculated for 30 days (G30) and inoculated for 90 days (G90). Rats from the G30 and G90 groups received an oral inoculum with 500 oocysts from a genotype III (M7741) T. gondii strain. At 180 days of age, all animals were anaesthetised and euthanised. Whole mounts were stained by using Giemsa (total population) and NADPH-diaphorase (nitrergic subpopulation) histochemistry. Maintenance of the width, length, area and neuronal density was observed; there was neuronal atrophy in the G30 group and a tendency to hypertrophy in the G90 group. Rats inoculated orally with sporulated oocysts did not show clinical illness or macroscopic or microscopic lesions, as do the majority of animal species. Therefore, infection was confirmed by a serum agglutination test; 30 days of infection caused increased weight gain and atrophy of myenteric neurons. At 90 days post-infection, weight gain became normal, and myenteric neurons hypertrophied.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Chronic infection with Toxoplasma gondii causes myenteric neuroplasticity of the jejunum in rats

Hermes-Uliana

Pereira-Severi

Luerdes

et al. 2011

Autonomic Neuroscience

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“…Enteral neural plasticity was also reported in other studies by our group, such as in myenteric neurons in the large intestine in chronic infection (genotype III strain), in the total population and nitrergic subpopulation of myenteric neurons in the jejunum in rats (ME‐49 strain), and in metabolically active myenteric neurons in the jejunum in rats that were infected for 24 h (M7741 strain) …”

Section: Discussionsupporting

confidence: 81%

“…9 We observed hypertrophy of the total neuron population, which occurred in myenteric neurons 24 hours after infection and submu- subpopulation of myenteric neurons in the jejunum in rats (ME-49 strain), 18 and in metabolically active myenteric neurons in the jejunum in rats that were infected for 24 h (M7741 strain). 43 No EGC loss was observed in the myenteric plexus. This preservation of EGCs may be attributable to glial resistance or a defense mechanism of these cells in an attempt to promote the maintenance of neurons after the establishment of parasitic infection.…”

Section: Discussionmentioning

confidence: 95%

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

Trevizan

Schneider

Araújo

et al. 2018

Neurogastroenterology Motil

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Background Toxoplasma gondii infection can occur through the ingestion of raw meat that contains tissue cysts or food that contains oocysts. Through the ingestion of oocysts, the parasite crosses the intestinal barrier, where the enteric nervous system is located. The objective was to investigate the kinetics of neuronal and glial responses during acute T. gondii infection. Methods We used 45 Wistar rats that were divided into a control group and infected groups that were evaluated at 6, 12, 24, 48, 72 hours, 7 days, 10 days, and 15 days after infection. The rats received 5000 sporulated oocysts of the parasite orally. To detect neurons and enteric glia cells, the myenteric and submucosal plexuses of the duodenum underwent double‐labeling immunohistochemical techniques to evaluate HuC/HuD and S100, HuC/HuD and ChAT, and HuC/HuD and nNOS. Key Results We observed a reduction of the total neuron population in the submucosal plexus 72 hours after infection. Cholinergic neurons decreased in the submucosal plexus 15 days after infection, and nitrergic neurons decreased in the myenteric plexus 72 hours after infection. A decrease in the number of glial cells was observed 7 days after infection in the submucosal plexus, and an increase in the enteric glial cell (EGC)/neuron ratio was found in both plexuses 48 hours after infection. Conclusions and Inferences We found decrease of neurons and increase in the EGC/neuron ratio in both plexuses caused by acute T. gondii infection, with major alterations 72 hours after oral infection. The number of cholinergic neurons decreased in the submucosal plexus, and the number of nitrergic neurons decreased in the myenteric plexus. A decrease in the number of enteric glial cells was observed in the submucosal plexus, and an increase in the enteric glial cell/neuron ratio was observed in both ganglionate plexuses of the duodenum.

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Acute infection with an avirulent strain of Toxoplasma gondii causes decreasing and atrophy of nitrergic myenteric neurons of rats

et al. 2017

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Hypertrophy of NADH-diaphorase positive myenteric neurons in rat jejunum after acute infection caused by Toxoplasma gondii

Cited by 10 publications

References 28 publications

Chronic infection with Toxoplasma gondii causes myenteric neuroplasticity of the jejunum in rats

Chronic infection with Toxoplasma gondii causes myenteric neuroplasticity of the jejunum in rats

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

Acute infection with an avirulent strain of Toxoplasma gondii causes decreasing and atrophy of nitrergic myenteric neurons of rats

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