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CX3CL1 在结膜中的表达参与了毒性眼表炎症期间免疫细胞的迁移。

CX3CL1 expression in the conjunctiva is involved in immune cell trafficking during toxic ocular surface inflammation.

机构信息

UPMC University Paris 6, Institut de la Vision, UMRS968, Paris, France.

出版信息

Mucosal Immunol. 2012 Nov;5(6):702-11. doi: 10.1038/mi.2012.43. Epub 2012 Jun 13.

DOI:10.1038/mi.2012.43
PMID:22692452
Abstract

Inappropriate expression of the chemokine CX3CL1 is reportedly known to act on inflammatory conditions in extraocular immune diseases. We studied the expression and effects of CX3CL1 in human patients, cultured human conjunctival cells, and transgenic mice exposed to benzalkonium chloride (BAC), a commonly used preservative in ophthalmic medications despite its proinflammatory properties, to determine whether CX3CL1 is involved in conjunctival inflammation. We report that CX3CL1 expression is increased in the conjunctiva of patients receiving BAC-containing medication, and correlates with clinical inflammation. BAC enhances the production of CX3CL1 in a conjunctival epithelial cell line, through the tumor-necrosis factor-α pathway, which attracts specific leukocyte subsets. In vivo, BAC-induced macrophage infiltration and subsequent inflammation of the conjunctiva is decreased in CX3CR1-deficient mice as compared with CX3CR1(+/+) controls. This translational study opens new avenue to investigate ocular surface disorders by focusing on chemokine-related inflammation and immune cell trafficking in the ocular conjunctival mucosa.

摘要

据报道,趋化因子 CX3CL1 的表达不当会影响眼外免疫疾病的炎症状态。我们研究了 CX3CL1 在人类患者、培养的人结膜细胞和接触苯扎氯铵(BAC)的转基因小鼠中的表达和作用,BAC 是一种常用于眼科药物的防腐剂,尽管它具有促炎特性。我们报告说,接受含 BAC 药物治疗的患者的结膜中 CX3CL1 的表达增加,并且与临床炎症相关。BAC 通过肿瘤坏死因子-α途径增强结膜上皮细胞系中 CX3CL1 的产生,该途径吸引特定的白细胞亚群。在体内,与 CX3CR1(+/+)对照相比,BAC 诱导的巨噬细胞浸润和随后的结膜炎症在 CX3CR1 缺陷型小鼠中减少。这项转化研究通过关注眼结膜黏膜中与趋化因子相关的炎症和免疫细胞迁移,为研究眼表面疾病开辟了新途径。

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