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慢性特发性荨麻疹患者外周血单个核细胞趋化因子 C-C 配体 2(CCL2)和 C-X-C 趋化因子 8(CXCL8)表达上调。

Up-regulation of chemokine C-C ligand 2 (CCL2) and C-X-C chemokine 8 (CXCL8) expression by monocytes in chronic idiopathic urticaria.

机构信息

Laboratory of Dermatology and Immunodeficiencies (LIM-56), Department of Dermatology, Medical School of University of São Paulo, São Paulo, Brazil.

出版信息

Clin Exp Immunol. 2012 Jan;167(1):129-36. doi: 10.1111/j.1365-2249.2011.04485.x.

Abstract

The disturbed cytokine-chemokine network could play an important role in the onset of diseases with inflammatory processes such as chronic idiopathic urticaria (CIU). Our main objectives were to evaluate the relation between proinflammatory chemokine serum levels from CIU patients and their response to autologous skin test (ASST) and basophil histamine release (BHR). We also aimed to assess the chemokine secretion by peripheral blood mononuclear cells (PBMC) upon polyclonal stimulus and to evaluate chemokine C-C ligand 2/C-X-C chemokine 8 (CCL2/CXCL8) and Toll-like receptor-4 (TLR-4) expression in monocytes. We observed significantly higher serum levels of the CXCL8, CXCL9, CXCL10 and CCL2 in CIU patients compared to the healthy group, regardless of the BHR or ASST response. The basal secretion of CCL2 by PBMC or induced by Staphylococcus aureus enterotoxin A (SEA) was higher in CIU patients than in the control group, as well as for CXCL8 and CCL5 secretions upon phytohaemagglutinin stimulation. Also, up-regulation of CCL2 and CXCL8 mRNA expression was found in monocytes of patients upon SEA stimulation. The findings showed a high responsiveness of monocytes through CCL2/CXCL8 expression, contributing to the creation of a proinflammatory environment in CIU.

摘要

紊乱的细胞因子-趋化因子网络可能在具有炎症过程的疾病(如慢性特发性荨麻疹)的发病中发挥重要作用。我们的主要目的是评估慢性特发性荨麻疹患者的促炎趋化因子血清水平与其对自身皮肤试验(ASST)和嗜碱性粒细胞组胺释放(BHR)反应之间的关系。我们还旨在评估外周血单核细胞(PBMC)在多克隆刺激下的趋化因子分泌,并评估趋化因子 C-C 配体 2/C-X-C 趋化因子 8(CCL2/CXCL8)和 Toll 样受体-4(TLR-4)在单核细胞中的表达。我们观察到,无论 BHR 或 ASST 反应如何,慢性特发性荨麻疹患者的血清 CXCL8、CXCL9、CXCL10 和 CCL2 水平明显高于健康组。慢性特发性荨麻疹患者的 PBMC 基础分泌或金黄色葡萄球菌肠毒素 A(SEA)诱导的 CCL2 分泌高于对照组,而植物血凝素刺激时 CXCL8 和 CCL5 的分泌也较高。此外,SEA 刺激后患者单核细胞中 CCL2 和 CXCL8 mRNA 表达上调。研究结果表明,单核细胞通过 CCL2/CXCL8 表达具有高度的反应性,有助于慢性特发性荨麻疹中促炎环境的形成。

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