Saxena Sandeep, Pant Aditya B, Khanna Vinay K, Agarwal A K, Singh Kamlesh, Kumar Dipak, Singh Vijay K
Department of Ophthalmology, King George's Medical University, Lucknow, India.
Ocul Immunol Inflamm. 2009 May-Jun;17(3):201-6. doi: 10.1080/09273940902731015.
Eales disease is an idiopathic obliterative vasculopathy that primarily affects the peripheral retina of young adults. The authors evaluated interleukin 1 beta (IL-1beta), interleukin-6 (IL-6), Interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-alpha) in the serum of patients with Eales disease stages for the first time.
The study group consisted of 45 consecutive patients of Eales disease [inflammatory stage (n = 15) and proliferative stage (n = 30)] and 28 healthy controls. Immunoassays for the quantification of the levels of four cytokines including IL-1beta, IL-6, IL-10, and TNF-alpha in the serum samples were performed using ELISA kits.
IL-1beta, IL-6, IL-10, and TNF-alpha levels were found to be increased significantly in the inflammatory stage of Eales disease as compared to controls (p < .001). IL-1beta levels decreased significantly during the proliferative stage of the disease as compared to the inflammatory stage (p = .03). TNF-alpha levels increased significantly during the proliferative stage as compared to the inflammatory stage (p = .02).
Raised levels of IL-1beta and TNF-alpha were observed in the inflammatory stage and persisted in the proliferative stage of the disease. The IL-1 system and TNF-alpha represent novel target for immunotherapy for controlling inflammatory activity and/or the associated long-term sequelae related to angiogenesis in Eales disease.
伊尔斯病是一种特发性闭塞性血管病,主要影响年轻成年人的周边视网膜。作者首次评估了不同阶段伊尔斯病患者血清中的白细胞介素1β(IL-1β)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)和肿瘤坏死因子-α(TNF-α)。
研究组由45例连续的伊尔斯病患者[炎症期(n = 15)和增殖期(n = 30)]以及28名健康对照组成。使用酶联免疫吸附测定(ELISA)试剂盒对血清样本中包括IL-1β、IL-6、IL-10和TNF-α在内的四种细胞因子水平进行定量免疫测定。
与对照组相比,发现伊尔斯病炎症期的IL-1β、IL-6、IL-10和TNF-α水平显著升高(p <.001)。与炎症期相比,疾病增殖期的IL-1β水平显著降低(p =.03)。与炎症期相比,增殖期的TNF-α水平显著升高(p =.02)。
在疾病的炎症期观察到IL-1β和TNF-α水平升高,并在增殖期持续存在。IL-1系统和TNF-α是控制伊尔斯病炎症活动和/或与血管生成相关的长期后遗症的免疫治疗新靶点。