Clinical Trials Study
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World J Diabetes. Apr 15, 2014; 5(2): 219-223
Published online Apr 15, 2014. doi: 10.4239/wjd.v5.i2.219
Toll-like receptor expression and signaling in human diabetic wounds
Mohan R Dasu, Sandra J Martin
Mohan R Dasu, Department of Dermatology, University of California at Davis, Davis, CA 95816, United States
Sandra J Martin, McClellan Outpatient Clinic, V A Northern California Health Care System, Sacramento, CA 95652, United States
Author contributions: All authors contributed to this work.
Correspondence to: Mohan R Dasu, PhD, Department of Dermatology, University of California at Davis, 3301 C Street, Sacramento, CA 95816, United States. ravi.dasu@ucdmc.ucdavis.edu
Telephone: +1-530-7528153 Fax: +1-530-7529766
Received: September 25, 2013
Revised: January 28, 2014
Accepted: March 17, 2014
Published online: April 15, 2014
Abstract

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.

Keywords: Interleukin-1β, Inflammation, Toll-like receptors 2, Toll-like receptors 4, Tumor necrosis factor-α, Type 2-diabetes mellitus, Wound healing

Core tip: Increased TLR2/4-MyD88-nuclear factor-kappa B expression and signaling with attendant oxidative stress may contribute to the hyperinflammation frequently seen in human diabetic wounds.