CYTOKINES IN PROLIFERATIVE DIABETIC-RETINOPATHY AND PROLIFERATIVE VITREORETINOPATHY

CYTOKINES IN PROLIFERATIVE DIABETIC-RETINOPATHY AND PROLIFERATIVE VITREORETINOPATHY
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DOI:
10.3109/02713689508998529
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发表时间:
1995-11-01
影响因子:
2
通讯作者:
STRIETER, RM
STRIETER, RM
中科院分区:
医学4区
文献类型:
--
作者:
ELNER, SG;ELNER, VM;STRIETER, RM

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我们确定白细胞介素-8,单核细胞趋化蛋白-1,巨噬细胞集落刺激因子是否存在于增生性糖尿病视网膜病变(PDR)或增生性玻璃体视网膜病变(PVR)患者的玻璃体中。这些细胞因子的水平通过特异性酶联免疫测定法在30例PDR患者、13例PVR患者和26例对照个体的Vitamin中进行测量,其中包括10例尸体眼和16例特发性黄斑裂孔、特发性黄斑皱褶、玻璃体破裂或单纯性视网膜脱离患者。白细胞介素-8的检测水平在90%的PDR患者,85%的PVR患者和58%的对照组玻璃体样本中发现。与对照人玻璃体(8.5 +/- 2.5 ng/ml)相比,PDR中的IL-8显著增加(平均值+/- SEM; 25.0 +/- 5.3 ng/ml; p = 0.01),但PVR中的IL-8没有显著增加(11.9 +/- 3.9 ng/ml; p = 0.50)。在PDR患者的90%的玻璃体样本中检测到MCP-1,PVR患者的99%的玻璃体样本中检测到MCP-1,对照样本的81%的玻璃体样本中检测到MCP-1。MCP-1在PDR(6.2 +/- 0.9 ng/ml,p = 0.001)和PVR(7.7 +/- 2.5 ng/ml,p = 0.001)中显著高于对照玻璃体中的水平(1.2 +/- 0.2 ng/ml)。在PDR患者的94%的玻璃体样本中检测到M-CSF,PVR患者为88%,对照玻璃体为92%。与对照组(10.7 +/- 3.5 ng/ml)相比,PDR组(32.3 +/- 8.3 ng/ml,p = 0.03)的M-CSF显著升高,但PVR组(23.6 +/- 12.8 ng/ml,p = 0.4)未显著升高。提示IL-8、MCP-1和M-CSF参与了PDR和PVR的发病机制。
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 ng/ml). MCP-I was detected in 90% of vitreous samples of patients with PDR, 99% 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.