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AIM: To examine the contribution of toll-like receptors(TLRs) expression and activation to the prolonged inflammation often seen in human diabetic wounds.METHODS: 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. RESULTS: 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). CONCLUSION: Collectively, our novel findings show that increased TLR expression, signaling, and activation may contribute to the hyper inflammation in the human diabetic wounds.
AIM: To examine the contribution of toll-like receptors (TLRs) expression and activation to the prolonged inflammation often seen in human diabetic wounds. METHODS: Debridement wound tissue was collected from diabetic patients with informed consent. Total RNA and protein were isolated and treated RESULTS: TLR1, 2, 4, and 6 mRNA expressions were significantly increased in wounds of diabetic patients compared with non-diabetic wounds (P <0.05). MyD88 protein expression was significantly increased in wounds of diabetic patients compared with non-diabetic wounds 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). CONCLUSION : Collectively, our novel findings show that increased TLR expression, signaling, and activation may contribute to the hyper inflammation in the human diab etic wounds.