Increased accumulation of advanced glycation end products (AGEs) in diabetic skin is closely related to delayed wound healing. Studies have shown that the concentration of AGEs is elevated in the skin tissues and not subcutaneous tissues in refractory diabetic wounds, which suggests there may be a causal relationship between the two. In the present study, experiments in human cells revealed that AGEs activated neutrophils, and the migratory and adhesive functions of neutrophils decreased once AGE levels reached a certain threshold. Neutrophils are a type of white blood cell (WBC or granulocyte) that protect us from infections, among other functions. They make up approximately 40% to 60% of the white blood cells in our bodies,1 and are the first cells to arrive on the scene when we experience a bacterial infection. Different levels of AGE expression differentially affected the function of neutrophils.
Conclusion: Neutrophils cannot effectively stimulate the formation of the inflammatory belt needed to remove necrotic tissues and defend against foreign microorganisms within diabetic chronic wounds. AGEs accumulate in different layers of the skin and can be activated for better ulcers healing.