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Enteromyxum spp.(粘孢子虫)感染对肠道 E-钙黏蛋白的调节作用:牙鲆对抗真鲷。

Effects of Enteromyxum spp. (Myxozoa) infection in the regulation of intestinal E-cadherin: Turbot against gilthead sea bream.

机构信息

Departamento de Anatomía, Producción Animal y Ciencias Clínicas Veterinarias, Universidade de Santiago de Compostela, Lugo, Spain.

Fish Pathology Group, Instituto de Acuicultura Torre de la Sal, Castellón, Spain.

出版信息

J Fish Dis. 2020 Mar;43(3):337-346. doi: 10.1111/jfd.13130. Epub 2020 Jan 26.

Abstract

Enteromyxoses are relevant diseases for turbot and gilthead sea bream aquaculture. The myxozoan parasites invade the intestinal mucosa, causing a cachectic syndrome associated with intestinal barrier alteration; nonetheless, their pathological impact is different. Turbot infected by Enteromyxum scophthalmi develop more severe intestinal lesions, reaching mortality rates of 100%, whereas in E. leei-infected gilthead sea bream, the disease progresses slowly, and mortality rates are lower. The mechanisms underlying the different pathogenesis are still unclear. We studied the distribution and expression changes of E-cadherin, a highly conserved protein of the adherens junctions, in the intestine of both species by immunohistochemistry and quantitative PCR, using the same immunohistochemical protocol and common primers. The regular immunostaining pattern observed in control fish turned into markedly irregular in parasitized turbot, showing an intense immunoreaction at the host-parasite interface. Nevertheless, E-cadherin gene expression was not significantly modulated in this species. On the contrary, no evident changes in the protein distribution were noticed in gilthead sea bream, whereas a significant gene downregulation occurred in advanced infection. The results contribute to the understanding of the different host-parasite interactions in enteromyxoses. Host and parasite cells appear to establish diverse relationships in these species, which could underlie the different pathological picture.

摘要

肠黏孢子虫病与大菱鲆和金头鲷养殖密切相关。黏孢子虫寄生虫侵袭肠道黏膜,引起与肠道屏障改变相关的恶病质综合征;然而,它们的病理影响不同。感染肠黏孢子虫的大菱鲆会发展出更严重的肠道病变,死亡率达到 100%,而感染 E. leei 的金头鲷,疾病进展缓慢,死亡率较低。导致不同发病机制的机制尚不清楚。我们通过免疫组织化学和定量 PCR 研究了黏孢子虫感染大菱鲆和金头鲷后,肠道中高度保守的黏附连接蛋白 E-钙黏蛋白的分布和表达变化,使用相同的免疫组织化学方案和常见引物。在对照组鱼类中观察到的规则免疫染色模式在感染的大菱鲆中变得明显不规则,在宿主-寄生虫界面显示出强烈的免疫反应。然而,在这种物种中,E-钙黏蛋白基因表达没有明显调节。相反,在金头鲷中没有发现蛋白质分布的明显变化,而在晚期感染中则发生了显著的基因下调。这些结果有助于了解肠黏孢子虫病中的不同宿主-寄生虫相互作用。宿主和寄生虫细胞似乎在这些物种中建立了不同的关系,这可能是导致不同病理表现的原因。

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