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刚地弓形虫慢性感染可导致大鼠黏膜下肠神经元死亡及结肠黏膜损伤。

Chronic infection with Toxoplasma gondii induces death of submucosal enteric neurons and damage in the colonic mucosa of rats.

作者信息

Góis Marcelo Biondaro, Hermes-Uliana Catchia, Barreto Zago Maísa Cristina, Zanoni Jacqueline Nelisis, da Silva Aristeu Vieira, de Miranda-Neto Marcílio Hubner, de Almeida Araújo Eduardo José, Sant'Ana Débora de Mello Gonçales

机构信息

State University of Maringa, Department of Morphological Sciences, Maringa, PR, Brazil.

Federal University of Mato Grosso do Sul, Department of Pharmacy, Coxim, MS, Brazil.

出版信息

Exp Parasitol. 2016 May;164:56-63. doi: 10.1016/j.exppara.2016.02.009. Epub 2016 Feb 21.

DOI:10.1016/j.exppara.2016.02.009
PMID:26902605
Abstract

Intestinal epithelial secretion is coordinated by the submucosal plexus (SMP). Chemical mediators from SMP regulate the immunobiological response and direct actions against infectious agents. Toxoplasma gondii is a worldwide parasite that causes toxoplasmosis. This study aimed to determine the effects of chronic infection with T. gondii on the morphometry of the mucosa and the submucosal enteric neurons in the proximal colon of rats. Male adult rats were distributed into a control group (n = 10) and an infected group (n = 10). Infected rats received orally 500 oocysts of T. gondii (ME-49). After 36 days, the rats were euthanized and samples of the proximal colon were processed for histology to evaluate mucosal thickness in sections. Whole mounts were stained with methylene blue and subjected to immunohistochemistry to detect vasoactive intestinal polypeptide. The total number of submucosal neurons decreased by 16.20%. Vasoactive intestinal polypeptide-immunoreactive neurons increased by 26.95%. Intraepithelial lymphocytes increased by 62.86% and sulfomucin-producing goblet cells decreased by 22.87%. Crypt depth was greater by 43.02%. It was concluded that chronic infection with T. gondii induced death and hypertrophy in the remaining submucosal enteric neurons and damage to the colonic mucosa of rats.

摘要

肠上皮分泌由黏膜下神经丛(SMP)协调。来自SMP的化学介质调节免疫生物学反应并直接对抗感染因子。刚地弓形虫是一种引起弓形虫病的全球寄生虫。本研究旨在确定大鼠近端结肠中慢性感染刚地弓形虫对黏膜形态计量学和黏膜下肠神经元的影响。成年雄性大鼠被分为对照组(n = 10)和感染组(n = 10)。感染大鼠口服500个刚地弓形虫卵囊(ME-49)。36天后,将大鼠安乐死,并对近端结肠样本进行组织学处理,以评估切片中的黏膜厚度。整装片用亚甲蓝染色并进行免疫组织化学检测血管活性肠肽。黏膜下神经元总数减少了16.20%。血管活性肠肽免疫反应性神经元增加了26.95%。上皮内淋巴细胞增加了62.86%,产生硫黏液的杯状细胞减少了22.87%。隐窝深度增加了43.02%。得出的结论是,慢性感染刚地弓形虫会导致大鼠剩余黏膜下肠神经元死亡和肥大以及结肠黏膜损伤。

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