Figure 1.

Composite tissue injuries involves multiple immune cells and endogenous immune pathways. Tissue-resident macrophages release chemoattractants triggering neutrophil infiltration and the simultaneous activation of complement pathway molecules in vessels. These events result in increased pro-inflammatory conditions with an increased number of M1-like macrophages. Pro-inflammatory arachidonic acid pathway metabolites, PGE2 and leukotrienes along with pro-inflammatory cytokines result in initiating precursor cells in various damaged tissues. An increase in Th2 immune response is established with an increase in IL10, IL4, and IL3, etc., which propagates M2 macrophages and Tregs that help in inducing cell differentiation and wound healing. A sustained pro-inflammatory reaction for a longer duration than needed results in a chronic wound or delayed wound closure.