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墨西哥 TcI 克氏锥虫株引起的胃肠道感染:不同程度的定殖和不同的免疫反应。

Gastrointestinal infection with Mexican TcI Trypanosoma cruzi strains: different degrees of colonization and diverse immune responses.

机构信息

Departamento de Inmunología. Instituto de Investigaciones Biomédicas. Universidad Nacional Autónoma de México, Mexico City 04510.

出版信息

Int J Biol Sci. 2011;7(9):1357-70. doi: 10.7150/ijbs.7.1357. Epub 2011 Nov 1.

Abstract

Mexican Ninoa and Queretaro (Qro) TcI strains of Trypanosoma cruzi have shown different degrees of virulence, and the two strains produce heterogeneous immune responses in the hearts of infected mice. This work shows that the same strains can invade the intestine by an intraperitoneal route and establish an infection, mainly in the colon. The three segments of the small intestine (duodenum, jejunum and ileum) were infected to a lesser degree than the colon. Despite the fact that parasites were predominantly found in the colon, an obvious inflammatory reaction was observed in the submucosal layer along the entire intestinal tract, with the virulent Qro strain causing significantly more areas of higher immune infiltration. A clear recruitment of CD4⁺ and CD8⁺ T lymphocytes to the mesenteric ganglia was observed during infection with the virulent strain. Macrophages were also differentially distributed in the gastrointestinal tract. These later cells infiltrated fewer amastigote nests in the mice infected with the Qro strain than in the mice infected with the Ninoa strain. When IFN-γ, TNF-α, and IL-4 levels were measured, an increase in these cytokines was observed compared with the uninfected mice. The role of these inflammatory reactions in the pathogenesis of Chagas enteropathy is also discussed in this paper.

摘要

墨西哥 Ninoa 和奎雷塔罗(Qro)TCI 株的克氏锥虫表现出不同程度的毒力,并且这两种株系在感染小鼠的心脏中产生异质的免疫反应。这项工作表明,相同的株系可以通过腹腔途径侵入肠道并建立感染,主要是在结肠。小肠的三个部分(十二指肠、空肠和回肠)感染程度小于结肠。尽管寄生虫主要存在于结肠中,但在整个肠道的黏膜下层观察到明显的炎症反应,毒力较强的 Qro 株导致更高免疫浸润区域显著增加。在感染强毒株时,明显观察到 CD4⁺和 CD8⁺T 淋巴细胞向肠系膜神经节的募集。巨噬细胞在胃肠道中的分布也不同。与感染 Ninoa 株的小鼠相比,感染 Qro 株的小鼠中浸润的巨噬细胞较少。与未感染的小鼠相比,当测量 IFN-γ、TNF-α 和 IL-4 水平时,这些细胞因子的水平增加。本文还讨论了这些炎症反应在恰加斯肠病发病机制中的作用。

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