Burn injury induces elevated inflammatory traffic: the role of NF-κB

A burn insult generally sustains a hypovolemic shock due to a significant loss of plasma from the vessels. The burn injury triggers the release of various mediators, such as reactive oxygen species (ROS), cytokines, and inflammatory mediators. Damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), stemming from foreign microbial discharge and damaged tissue or necrotic cells from the burn-injured site, enter the systemic circulation, activate toll-like receptors (TLRs), and trigger the excessive secretion of cytokines and inflammatory mediators. Inflammation plays a vital role in remodeling an injured tissue, detoxifying toxins, and helps in the healing process. A transcription factor, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), contributes to a variety of physiological and pathological conditions, including immune response, cell death, cell survival, and inflammatory processes. During the pathogenesis of a burn wound, upregulation of various cytokines and growth factors lead to undesirable tissue inflammation. Thus, NF-κB, a dominant moderator of inflammation, needs to be altered to prove beneficial to the treatment of burns or other inflammation-associated diseases. This review addresses the relationship between NF-κB and elevated inflammation in a burn condition that could potentially be altered to induce an early wound-healing mechanism of burn wounds.