急性闭角型青光眼发病机制与Toll样受体及髓样分化因子88免疫调节作用的相关性分析

目的探讨急性原发性闭角型青光眼(PACG)发病机制与Toll样受体(TLR)及髓样分化因子88(My D88)免疫调节作用的相关性,为临床治疗提供依据。方法选取2015年1月至2015年12月收入我院的90例急性PACG患者为研究组,根据视野损伤程度将患者分为重、中、轻三个亚组,选取同期入院的32例白内障患者为对照组,统计两组患者的基线资料,并检测两组患者的TLR4、My D88蛋白及炎性因子(IL-2、IL-6)的表达水平。结果两组患者TLR4和My D88的蛋白表达水平比较,具有统计学差异(P<0.05),且视神经损伤重度组的TLR4和My D88的蛋白表达水平显著高于视神经损伤中度组及视神经损伤轻度组,具有统计学差异(P<0.05)。两组患者外周血IL-2及IL-6水平比较,具有统计学差异(P<0.05),视神经损伤重度组的IL-2水平与视神经损伤中度组相比较,无统计学差异(P>0.05),但其显著低于视神经损伤轻度组,具有统计学差异(P<0.05);视神经损伤重度组的IL-6水平与视神经损伤中度组及视神经损伤轻度组相比较,均无统计学差异(P>0.05)。结论急性PACG的发病可能与TLR4和My D88的免疫调节有关,急性PACG发作期虹膜组织发生炎症,且TLR4和My D88的表达水平升高,这一过程依照TLR4-My D88的信号传导。

Roles of Toll-like receptor and myeloid differentiation factor 88 in the pathogenesis of acute angle-closure glaucoma

Objective To investigate the roles of TLR4 MyD88-dependent signaling pathways in the pathogenesis of acute angle-closure glaucoma. To find an effective way to prevent and treat acute angle-closure glaucoma. Methods Hospitalized patients with primary acute angle-closure glaucoma in the Department of Ophthalmology from January,2015 to December,2015 were recruited. Patients were divided into three subgroups according to the degree of optic nerve injury (minor,medium or severe). Patients with cataract who hospitalized within the same period were selected as the control group. Western blot was used to detect TLR4 and MyD88 receptor protein expression in iris. Serum concentrations of IL-2 and IL-6 were also measured. Results Western blot showed that expression of TLR4 and MyD88 was significantly higher in glaucoma patients (P < 0. 05). Concentrations of TLR4 and MyD88 in glaucoma patients with severe optic nerve injury were significantly higher than those who had mild optic nerve injury (P < 0. 05). IL - 2 and IL - 6 were significantly lower than in glaucoma patients (P < 0. 05),and was lowest in patients with severe optic nerve injury. Conclusions Acute an-gle-closure glaucoma patients showed evidence of septic inflammation reactions in iris. Expression of TLR4 and MyD88 sig-nificantly increased,indicating acute inflammatory attack. TLR4-MyD88-dependent signaling pathways play an important role in the pathogenesis of acute angle-closure glaucoma.