International Ocular Surface Research Center, Institute of Ophthalmology and Key Laboratory for Regenerative Medicine, Jinan University, Guangzhou, China.
International Ocular Surface Research Center, Institute of Ophthalmology and Key Laboratory for Regenerative Medicine, Jinan University, Guangzhou, China; Department of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Am J Pathol. 2020 Jun;190(6):1298-1308. doi: 10.1016/j.ajpath.2020.02.004. Epub 2020 Mar 16.
Eosinophils are a major cause of tissue injury in allergic conjunctivitis. The biological nature of eosinophils in the conjunctiva and the mechanisms that control eosinophils' responses in allergic conjunctivitis are currently not completely understood. This study reports that conjunctival eosinophils comprise two populations-Siglec-F and Siglec-F-in different life stages. Siglec-F eosinophils partly expressed CD34 and were in the immature (or steady) state. Siglec-F eosinophils did not express CD34, sharply increased in number after short ragweed (SRW) pollen challenge, and were in the mature (or activated) state. Moreover, chemical sympathectomy by 6-hydroxydopamine reduced the recruitment and activation of eosinophils, whereas the activation of the sympathetic nerve system (SNS) with restraint stress accelerated the recruitment and activation of eosinophils in SRW-induced conjunctivitis. It was also found that two eosinophil populations expressed alpha-1a-adrenergic receptors (α1a-ARs); in SRW-induced conjunctivitis, treatment with an α1a-AR antagonist decreased eosinophil responses, whereas treatment with an α1a-AR agonist aggravated eosinophil responses. Thus, eosinophil responses in conjunctivitis are regulated by the SNS via α1a-AR signaling. SNS inputs or α1a-AR function may be potential targets for the treatment of allergic conjunctivitis.
嗜酸性粒细胞是过敏性结膜炎组织损伤的主要原因。目前尚不完全了解结膜中嗜酸性粒细胞的生物学特性以及控制其在过敏性结膜炎中反应的机制。本研究报告称，结膜嗜酸性粒细胞包含两个群体——Siglec-F 和 Siglec-F，处于不同的生命阶段。Siglec-F 嗜酸性粒细胞部分表达 CD34，处于未成熟（或静止）状态。Siglec-F 嗜酸性粒细胞不表达 CD34，在短豚草花粉（SRW）挑战后数量急剧增加，处于成熟（或激活）状态。此外，通过 6-羟多巴胺进行化学交感神经切除术可减少嗜酸性粒细胞的募集和激活，而通过束缚应激激活交感神经系统（SNS）可加速 SRW 诱导的结膜炎中嗜酸性粒细胞的募集和激活。还发现两个嗜酸性粒细胞群体表达 alpha-1a-肾上腺素能受体（α1a-AR）；在 SRW 诱导的结膜炎中，用 α1a-AR 拮抗剂治疗可降低嗜酸性粒细胞反应，而用 α1a-AR 激动剂治疗则加重嗜酸性粒细胞反应。因此，结膜炎中的嗜酸性粒细胞反应受 SNS 通过α1a-AR 信号调节。SNS 输入或α1a-AR 功能可能是治疗过敏性结膜炎的潜在靶点。
