Literature DB >> 22804764

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

Débora M G Sant'Ana1, Marcelo B Góis, Jacqueline N Zanoni, Aristeu V da Silva, Cleverton J T da Silva, Eduardo J A Araújo.   

Abstract

Toxoplasma gondii (T. gondii) crosses the intestinal barrier in oral infections and can lead to changes in different cell types, including the neurons located there. In the gastrointestinal system, the autonomous nervous system component that regulate blood flow and mucous secretion is the submucosal plexus. The aim of this study was to examine the effects of T. gondii infection on intraepithelial lymphocytes (IELs), goblet cells and submucosal neurons that are immunoreactive to vasoactive intestinal peptide (VIP-IR) of rat jejunum. Twenty male rats distributed as a control group (CG) and an infected group (IG), which received a suspension with 500 parasite oocysts (strain ME-49, genotype II) orally, were assessed. Routine histological sections were used to quantify IELs and to detect mucins secreted by goblet cells. Whole mounts including the submucosal layer were examined using immunofluorescence to detect the VIP neurotransmitter. Quantitative alterations in IELs were not observed. However, the reduction (P < 0.05) in the number of goblet cells that produce neutral mucins (PAS+) and sulphomucins (AB pH 1.0) and the maintenance of sialomucin-secreting cells (AB pH 2.5) resulting in a more fluid mucous were observed. Concerning the VIP-IR submucosal neurons, an increase in fluorescence on IG animals was observed. There was a reduction (P < 0.05) in the number of VIP-IR submucosal neurons and atrophy of their cell bodies in IG rats. Infection with T. gondii caused alterations in the chemical composition of the intestinal mucous and reduction in the neuron number and atrophy of the remaining neurons in this cell subpopulation.
© 2012 The Authors. International Journal of Experimental Pathology © 2012 International Journal of Experimental Pathology.

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Year:  2012        PMID: 22804764      PMCID: PMC3444984          DOI: 10.1111/j.1365-2613.2012.00824.x

Source DB:  PubMed          Journal:  Int J Exp Pathol        ISSN: 0959-9673            Impact factor:   1.925


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