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通过实时逆转录聚合酶链反应对患有慢性肠病的犬十二指肠黏膜中的细胞因子mRNA进行定量分析。

Cytokine mRNA quantification in duodenal mucosa from dogs with chronic enteropathies by real-time reverse transcriptase polymerase chain reaction.

作者信息

Peters Iain R, Helps Chris R, Calvert Emma L, Hall Edward J, Day Michael J

机构信息

School of Clinical Veterinary Science, University of Bristol, Langford House, Langford, Bristol BS40 5DU, UK.

出版信息

J Vet Intern Med. 2005 Sep-Oct;19(5):644-53. doi: 10.1892/0891-6640(2005)19[644:cmqidm]2.0.co;2.

Abstract

The pathogenesis of inflammatory bowel disease (IBD) and antibiotic-responsive diarrhea (ARD) in dogs likely involves an interaction between the intestinal immune system and luminal bacterial or food antigens. German Shepherd Dogs (GSD) are particularly predisposed to both IBD and ARD. CD4+ T cells are important for the regulation of immune responses in the mucosa, and they exert their effects through the secretion of cytokines. The present study examined the role of cytokines in the pathogenesis of canine chronic enteropathies by quantification of mRNA encoding interleukin-2 (IL-2), IL-4, IL-5, IL-6, IL-10, IL-12, IL-18, interferon gamma, tumor necrosis factor-alpha, transforming growth factor-beta, and glyceraldehyde-3-phosphate dehydrogenase by real-time reverse transcriptase polymerase chain reaction in duodenal mucosal biopsies obtained from 39 dogs with chronic diarrhea and 18 control dogs. Contemporaneously collected biopsies were assessed for histologic changes with a 4-point grading system. No significant difference in the expression of cytokine mRNA (P > .01) was detected between dogs with and those without chronic diarrhea. Similarly, no significant differences in cytokine mRNA expression were observed between GSD and other breeds with chronic diarrhea, or between histologically normal duodenal mucosa and that with evidence of inflammatory change. Failure to detect a difference in mRNA expression does not rule out the possibility of a defect downstream at the level of translation or protein function. No conclusion can be drawn from these data as to the predominant CD4+ cell type in the pathogenesis of these canine chronic enteropathies.

摘要

犬类炎症性肠病(IBD)和抗生素反应性腹泻(ARD)的发病机制可能涉及肠道免疫系统与管腔细菌或食物抗原之间的相互作用。德国牧羊犬(GSD)尤其易患IBD和ARD。CD4 + T细胞对黏膜免疫反应的调节很重要,它们通过分泌细胞因子发挥作用。本研究通过实时逆转录聚合酶链反应对39只患有慢性腹泻的犬和18只对照犬十二指肠黏膜活检组织中编码白细胞介素-2(IL-2)、IL-4、IL-5、IL-6、IL-10、IL-12、IL-18、干扰素γ、肿瘤坏死因子-α、转化生长因子-β和甘油醛-3-磷酸脱氢酶的mRNA进行定量,以研究细胞因子在犬慢性肠病发病机制中的作用。同时收集的活检组织用4分制分级系统评估组织学变化。患有和未患有慢性腹泻的犬之间,细胞因子mRNA表达无显著差异(P>.01)。同样,GSD与其他患有慢性腹泻的犬种之间,以及组织学正常的十二指肠黏膜与有炎症变化迹象的十二指肠黏膜之间,细胞因子mRNA表达也无显著差异。未能检测到mRNA表达的差异并不排除在翻译或蛋白质功能水平下游存在缺陷的可能性。关于这些犬慢性肠病发病机制中主要的CD4 +细胞类型,从这些数据中无法得出结论。

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