Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogen Biology and Immunology, Jiangsu International Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou, Jiangsu, China.
The First Clinical Medical College, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Front Immunol. 2023 Jan 13;13:1084203. doi: 10.3389/fimmu.2022.1084203. eCollection 2022.
The intestinal tract serves as a critical regulator for nutrient absorption and overall health. However, its involvement in anti-parasitic infection and immunity has been largely neglected, especially when a parasite is not transmitted orally. The present study investigated the colonic histopathology and functional reprogramming in mice with intraperitoneal infection of the larval ().
Compared with the control group, the -infected mice exhibited deteriorated secreted mucus, shortened length, decreased expression of tight junction proteins zonula occludens-1 (ZO-1), and occludin in the colon. Moreover, RNA sequencing was employed to characterize colonic gene expression after infection. In total, 3,019 differentially expressed genes (1,346 upregulated and 1,673 downregulated genes) were identified in the colon of infected mice. KEGG pathway and GO enrichment analysis revealed that differentially expressed genes involved in intestinal immune responses, infectious disease-associated pathways, metabolism, or focal adhesion were significantly enriched. Among these, 18 tight junction-relative genes, 44 immune response-associated genes, and 23 metabolic genes were annotated. Furthermore, mebendazole treatment could reverse the colonic histopathology induced by infection.
Intraperitoneal infection with induced the pathological changes and functional reprogramming in the colon of mice, and mebendazole administration alleviated above alternations, highlighting the significance of the colon as a protective barrier against parasitic infection. The findings provide a novel perspective on host-parasite interplay and propose intestine as a possible target for treating parasitic diseases that are not transmitted orally.
肠道是营养吸收和整体健康的关键调节剂。然而，其在抗寄生虫感染和免疫中的作用在很大程度上被忽视了，尤其是当寄生虫不是通过口服传播时。本研究调查了腹腔内感染幼虫（）的小鼠的结肠组织病理学和功能重编程。
与对照组相比，感染组小鼠的分泌黏液恶化，结肠长度缩短，紧密连接蛋白闭合蛋白-1（ZO-1）和闭合蛋白的表达减少。此外，还采用 RNA 测序来描述感染后结肠基因表达。总共在感染小鼠的结肠中鉴定出 3019 个差异表达基因（1346 个上调和 1673 个下调基因）。KEGG 途径和 GO 富集分析表明，差异表达基因参与肠道免疫反应、传染病相关途径、代谢或焦点粘附等途径显著富集。其中，18 个紧密连接相关基因、44 个免疫反应相关基因和 23 个代谢基因被注释。此外，甲苯咪唑治疗可逆转感染引起的结肠组织病理学改变。
腹腔内感染导致小鼠结肠发生病理变化和功能重编程，甲苯咪唑治疗可减轻上述改变，这突显了结肠作为对抗寄生虫感染的保护性屏障的重要性。这些发现为宿主-寄生虫相互作用提供了新的视角，并提出了肠道可能是治疗非口服传播寄生虫病的潜在靶点。
