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犬肛门疖病病变中基质金属蛋白酶mRNA的表达

Matrix metalloproteinase mRNA expression in canine anal furunculosis lesions.

作者信息

House A K, Catchpole B, Gregory S P

机构信息

Department of Veterinary Clinical Sciences, Royal Veterinary College, University of London, Hawkshead Lane, North Mymms, Hertfordshire AL9 7TA, United Kingdom.

出版信息

Vet Immunol Immunopathol. 2007 Jan 15;115(1-2):68-75. doi: 10.1016/j.vetimm.2006.10.018. Epub 2006 Nov 27.

Abstract

Although the aetiology of anal furunculosis (AF) in dogs is poorly understood, there is evidence for an underlying immune dysfunction. This is illustrated by the presence of a T helper type 1 cytokine mRNA profile in AF lesions and the clinical response to ciclosporin therapy. Expression of MMPs 2, 9 and 13 were evaluated in AF lesional biopsies by real-time quantitative RT-PCR. There was significantly increased expression of both MMP-9 and MMP-13 mRNA in AF biopsies compared to controls (p<0.001) but no significant difference in MMP-2 mRNA expression. Since MMP-9 and MMP-13 are primarily produced by macrophages, these data suggest that ulceration could be the result of aberrant activation of this cell type in the tissues. It is feasible that such pathological macrophage activity occurs in response to interferon-gamma secreted by T helper type 1 cells. This could explain why the lesions resolve following treatment with the immunosuppressive drug ciclosporin.

摘要

尽管犬肛门疖病(AF)的病因尚不清楚,但有证据表明存在潜在的免疫功能障碍。AF病变中辅助性T细胞1型细胞因子mRNA谱的存在以及对环孢素治疗的临床反应都说明了这一点。通过实时定量逆转录聚合酶链反应(RT-PCR)评估AF病变活检组织中基质金属蛋白酶(MMP)2、9和13的表达。与对照组相比,AF活检组织中MMP-9和MMP-13 mRNA的表达均显著增加(p<0.001),但MMP-2 mRNA表达无显著差异。由于MMP-9和MMP-13主要由巨噬细胞产生,这些数据表明溃疡可能是该组织中这种细胞类型异常激活的结果。这种病理性巨噬细胞活性可能是对辅助性T细胞1型细胞分泌的干扰素-γ的反应。这可以解释为什么用免疫抑制药物环孢素治疗后病变会消退。

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