Biochemical mediators of inflammation and basic principles of wound healing in the skin

Abstract

Biochemical mediators released during inflammation intensify and propagate the inflammatory response. These mediators are soluble, diffusible molecules that can act locally and systemically. Mediators derived from plasma include complement and complement-derived peptides and kinins. Released via the classic or alternative pathways of the complement cascade, complement-derived peptides (C3a, C3b, and C5a) increase vascular permeability, cause smooth muscle contraction, activate leukocytes, and induce mast-cell degranulation. C5a is a potent chemotactic factor for neutrophils and mononuclear phagocytes. The kinins are also important inflammatory mediators. The most important kinin is bradykinin, which increases vascular permeability and vasodilation and, importantly, activates phospholipase A2 (PLA2) to liberate arachidonic acid (AA). Here, we review mediators of inflammation and process of wound healing.