Modulation of Inflammatory Dynamics by Insulin to Promote Wound Recovery of Diabetic Ulcers

Abstract

About 5% of the world population is diabetic and are at a risk of slow nonrecoverable wound formation. Estimated 15–25% of diabetic patients develop foot ulcers, 6% among them needing clinical attention among which 15–20% will need an amputation. This counts for around 50% of all traumatic amputation. Wound leads to activation of dynamic inflammatory cascade responsible for the healing process. But in diabetes, a persistent rise of pro-inflammatory cytokines and low anti-inflammatory cytokines blocks the dynamic cascade. Wounding induces various pro-inflammatory cytokines such as IL-1, IL-6, IL-12, IL-18, IFN-γ, and TNFs causing accumulation of free radicals leading to inflammation which become persistent in diabetes. Inhibition of proinflammatory cytokines drives the equilibrium towards the expression of anti-inflammatory cytokines such as IL4, IL-10, IL-11, IL-13, IFN-α, and TGF-β, which is necessary for the wound recovery process. Here in this chapter, the inflammatory modulatory roles of different drugs/formulations have been discussed to unravel their significance to promote wound recovery.