Elner S G, Elner V M, Jaffe G J, Stuart A, Kunkel S L, Strieter R M
Department of Ophthalmology, University of Michigan, Ann Arbor 48105, USA.
Curr Eye Res. 1995 Nov;14(11):1045-53. doi: 10.3109/02713689508998529.
We determined whether interleukin-8, monocyte chemotactic protein-1, and macrophage-colony stimulating factor are present in the vitreous of patients with proliferative diabetic retinopathy (PDR) or proliferative vitreoretinopathy (PVR). The levels of these cytokines were measured by specific enzyme-linked immunoassays in vitreous from 30 patients with PDR, 13 patients with PVR, and 26 control individuals, including 10 cadaver eyes and 16 patients with idiopathic macular holes, idiopathic macular puckers, vitreous hemorrhages, or uncomplicated retinal detachments. Detectable levels of interleukin-8 were found in 90% of vitreous samples of patients with PDR, 85% with PVR, and 58% of control samples. IL-8 was significantly increased in PDR (mean +/- SEM; 25.0 +/- 5.3 ng/ml; p = 0.01), but not in PVR (11.9 +/- 3.9 ng/ml; p = 0.50) compared to control human vitreous (8.5 +/- 2.5 2.5 ng/ml). MCP-1 was detected in 90% of vitreous samples of patients with PDR, 92% with PVR, and 81% of control samples. MCP-1 was significantly increased in PDR (6.2 +/- 0.9 ng/ml, p = 0.001) and PVR (7.7 +/- 2.5 ng/ml, p = 0.001) over the levels in control vitreous (1.2 +/- 0.2 ng/ml). M-CSF was detected in 94% of vitreous samples of patients with PDR, 88% with PVR, and 92% from control vitreous. M-CSF was significantly elevated in PDR (32.3 +/- 8.3 ng/ml, p = 0.03), but not in PVR (23.6 +/- 12.8 ng/ml, p = 0.4) compared to control (10.7 +/- 3.5 ng/ml). Our results suggest that IL-8, MCP-1, and M-CSF participate in the pathogenesis of PDR and PVR.
我们测定了增殖性糖尿病视网膜病变(PDR)或增殖性玻璃体视网膜病变(PVR)患者玻璃体内是否存在白细胞介素-8、单核细胞趋化蛋白-1和巨噬细胞集落刺激因子。通过特异性酶联免疫分析法检测了30例PDR患者、13例PVR患者以及26名对照者(包括10只尸体眼和16例患有特发性黄斑裂孔、特发性黄斑皱襞、玻璃体积血或单纯性视网膜脱离的患者)玻璃体内这些细胞因子的水平。在90%的PDR患者玻璃体液样本、85%的PVR患者玻璃体液样本以及58%的对照样本中检测到了可检测水平的白细胞介素-8。与对照人玻璃体(8.5±2.5 ng/ml)相比,PDR患者玻璃体内IL-8显著升高(平均值±标准误;25.0±5.3 ng/ml;p = 0.01),而PVR患者玻璃体内未升高(11.9±3.9 ng/ml;p = 0.50)。在90%的PDR患者玻璃体液样本、92%的PVR患者玻璃体液样本以及81%的对照样本中检测到了MCP-1。与对照玻璃体(1.2±0.2 ng/ml)水平相比,PDR患者(6.2±0.9 ng/ml,p = 0.001)和PVR患者(7.7±2.5 ng/ml,p = 0.001)玻璃体内MCP-1显著升高。在94%的PDR患者玻璃体液样本、88%的PVR患者玻璃体液样本以及92%的对照玻璃体样本中检测到了M-CSF。与对照(10.7±3.5 ng/ml)相比,PDR患者玻璃体内M-CSF显著升高(32.3±8.3 ng/ml,p = 0.03),而PVR患者玻璃体内未升高(23.6±12.8 ng/ml,p = 0.4)。我们的结果表明,IL-8、MCP-1和M-CSF参与了PDR和PVR的发病机制。