Mohan R Dasu, Department of Dermatology, University of California at Davis, Davis, CA 95816, United States.
World J Diabetes. 2014 Apr 15;5(2):219-23. doi: 10.4239/wjd.v5.i2.219.
To examine the contribution of toll-like receptors (TLRs) expression and activation to the prolonged inflammation often seen in human diabetic wounds.
Debridement wound tissue was collected from diabetic patients with informed consent. Total RNA and protein were isolated and subjected to real-time polymerase chain reaction and Western blot analyses.
TLR1, 2, 4, and 6 mRNA expressions were increased significantly in wounds of diabetic patients compared with non-diabetic wounds (P < 0.05). MyD88 protein expression was significantly increased in diabetic wounds compared to non-diabetic wounds. Interleukin-1beta, tumor necrosis factor-alpha concentration nuclear factor-kappa B activation, and thiobarbituric acid reactive substances were increased in diabetic wounds compared to non-diabetic wounds (P < 0.01).
Collectively, our novel findings show that increased TLR expression, signaling, and activation may contribute to the hyper inflammation in the human diabetic wounds.
探讨 Toll 样受体（TLRs）表达和激活对人类糖尿病性伤口中常见的长期炎症的贡献。
征得知情同意后，从糖尿病患者的清创伤口组织中采集总 RNA 和蛋白质，并进行实时聚合酶链反应和 Western blot 分析。
与非糖尿病性伤口相比，糖尿病患者的伤口中 TLR1、2、4 和 6 的 mRNA 表达显著增加（P < 0.05）。与非糖尿病性伤口相比，糖尿病伤口中 MyD88 蛋白表达显著增加。与非糖尿病性伤口相比，糖尿病伤口中白细胞介素-1β、肿瘤坏死因子-α浓度核因子-κB 激活和硫代巴比妥酸反应物质增加（P < 0.01）。
综上所述，我们的新发现表明，TLR 表达、信号转导和激活的增加可能导致人类糖尿病性伤口中的过度炎症。
