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肠黏膜中少年特发性关节炎患者热休克蛋白表达水平较低:免疫调节缺陷?

Heat shock protein expression is low in intestinal mucosa in juvenile idiopathic arthritis: a defect in immunoregulation?

机构信息

Department of Paediatrics, University of Oulu, and Oulu University Hospital, Oulu, Finland.

出版信息

Scand J Rheumatol. 2010 May;39(3):212-8. doi: 10.3109/03009740903390145.

Abstract

OBJECTIVES

Heat shock proteins (HSPs) are involved in the regulation of inflammation and in the maintenance of mucosal integrity. Their altered expression may be a marker of mucosal inflammation and also contribute to tissue injury. The small intestinal mucosa in children with juvenile idiopathic arthritis (JIA) shows signs of intestinal immune activation, such as increased intraepithelial cytotoxic lymphocyte counts. To further evaluate the characteristics of this immune activation in JIA, we have studied the expression of several HSPs, major histocompatibility complex (MHC) class I-related chain A (MICA), and the heat shock transcription factor 1 (HSF1) in intestinal biopsies from children with JIA.

METHODS

We studied 15 patients with JIA. Controls included 13 children without JIA, studied for various gastrointestinal (GI) symptoms, but eventually shown not to have any GI disease. The subjects were examined by endoscopy. The expression of HSP60, HSP70, MICA, and HSF1 was analysed in ileal and duodenal biopsies by using immunohistochemistry.

RESULTS

The expression levels of HSP60, MICA, and HSF1 were significantly lower in the duodenal epithelium in the JIA patients compared to the controls. MICA and HSF1 also showed lower expression in the ileal epithelium. The expression of HSP70 did not differ between the groups.

CONCLUSIONS

The downregulation of HSP60, MICA, and HSF1 in small intestinal mucosa may indicate that intestinal epithelial cells show immune aberration in JIA. We speculate that the low heat shock response may play a role in the pathogenesis of JIA, interfering with mucosal integrity and local intestinal immunoregulation.

摘要

目的

热休克蛋白(HSPs)参与炎症调节和黏膜完整性维持。其表达改变可能是黏膜炎症的标志物,也可能导致组织损伤。幼年特发性关节炎(JIA)患儿的小肠黏膜显示出肠道免疫激活的迹象,例如上皮内细胞毒性淋巴细胞计数增加。为了进一步评估 JIA 中这种免疫激活的特征,我们研究了 JIA 患儿肠道活检中几种 HSPs、主要组织相容性复合体(MHC)I 类相关链 A(MICA)和热休克转录因子 1(HSF1)的表达。

方法

我们研究了 15 名 JIA 患儿。对照组包括 13 名无 JIA 的儿童,因各种胃肠道(GI)症状而接受检查,但最终未发现任何 GI 疾病。通过内镜检查对受试者进行检查。通过免疫组织化学分析,在回肠和十二指肠活检中分析 HSP60、HSP70、MICA 和 HSF1 的表达。

结果

与对照组相比,JIA 患儿的十二指肠上皮中 HSP60、MICA 和 HSF1 的表达水平明显降低。MICA 和 HSF1 在回肠上皮中的表达也较低。两组之间 HSP70 的表达没有差异。

结论

小肠黏膜中 HSP60、MICA 和 HSF1 的下调可能表明 JIA 中的肠上皮细胞存在免疫异常。我们推测低热休克反应可能在 JIA 的发病机制中起作用,干扰黏膜完整性和局部肠道免疫调节。

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