Intraepithelial lymphocytes, goblet cells and VIP‐IR submucosal neurons of jejunum rats infected with <i>Toxoplasma gondii</i>

Sant’Ana, Débora de Mello Gonçales; Góis, Marcelo Biondaro; Zanoni, Jacqueline Nelisis; Silva, Aristeu Vieira da; Silva, Cleverton J T da; Araújo, Eduardo J.A.

doi:10.1111/j.1365-2613.2012.00824.x

Cited by 25 publications

(25 citation statements)

References 63 publications

(68 reference statements)

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“…Our previous studies have shown that the infection can cause changes in enteric neurons and in intestinal wall (da Silva Pde et al, 2010;Hermes-Uliana et al, 2011;Odorizzi et al, 2010;Sant'Ana et al, 2012;Shiraishi et al, 2009;Sugauara et al, 2008Sugauara et al, , 2009). These changes depend on the parasitic stage ingested, the duration of the infection, the host species and the part of the gastrointestinal tract evaluated.…”

Section: Introductionmentioning

confidence: 93%

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

Vicentino-Vieira

Melo

Góis

et al. 2015

Experimental Parasitology

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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.

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Section: Introductionmentioning

confidence: 93%

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

Vicentino-Vieira

Melo

Góis

et al. 2015

Experimental Parasitology

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“…Our research group has sought to understand this relationship for more than a decade. 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 .…”

Section: Introductionmentioning

confidence: 75%

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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“…In rats, after oral infection with T. gondii oocysts, Sant'Ana et al [507] found a marked reduction in the number of goblet cells producing neutral mucins (PAS+) and sulphomucins (AB pH 1.0) as compared with control animals, and these changes reflected production of a more fluid mucous (Table 34). The number of vasoactive intestinal peptide (VIP-IR) submucosal neurons as well as the area of the VIP-IR neuronal cell bodies also decreased significantly compared with control rats (667 ± 6.98 vs. 856 ± 14.89 per 1.74 mm 2 of the jejunum, p<0.05, and 317.29 ± 9.28 vs. 404.24 ± 11.10 µm 2 , p<0.05, respectively).…”

Section: T Gondii Infectionmentioning

confidence: 99%

“…The number of vasoactive intestinal peptide (VIP-IR) submucosal neurons as well as the area of the VIP-IR neuronal cell bodies also decreased significantly compared with control rats (667 ± 6.98 vs. 856 ± 14.89 per 1.74 mm 2 of the jejunum, p<0.05, and 317.29 ± 9.28 vs. 404.24 ± 11.10 µm 2 , p<0.05, respectively). All these abnormalities indicated that oral T. gondii infection caused alterations in the chemical composition of the intestinal mucous and reduction in the number of submucosal neurons associated with atrophy of the remaining neurons in this cell subpopulation [507]. In this context, it is suggested that the morphological changes reported in duodenal atresia (a well known neonatal intestinal disease), such as the neuronal cells decreased in number and size, the circular musculature moderately-to-severely hypertrophic, and the interstitial cells of Cajal decreased even around the myenteric plexus [508], were due to chronic latent T. gondii infection.…”

Section: T Gondii Infectionmentioning

confidence: 99%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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Intraepithelial lymphocytes, goblet cells and VIP‐IR submucosal neurons of jejunum rats infected with Toxoplasma gondii

Cited by 25 publications

References 63 publications

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

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

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

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

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