ABSTRACT
In a normal inammatory response, tissue injury triggers mast cells and resident macrophages to release pro-inammatory mediators such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, histamines, prostaglandins, and leukotrienes into the surrounding area, resulting in vasodilation and leaky blood vessels. Plasma proteins called complement are released and summon phagocytic cells, namely monocytes and neutrophils, to the area to remove necrotic tissue, invading bacteria, and debris. The œnal stage of inammation is resolution, where neutrophils convert prostaglandins and leukotrienes to lipoxins-initiating the termination sequence while alternatively activated macrophages produce anti-inammatory factors such as transforming growth factor (TGF)-β and IL-10. Neutrophils apoptose and reparative œbroblasts inœltrate the area to release matrix metalloproteinases (MMPs) for tissue remodeling while producing extracellular matrix (ECM) and collagen. Finally, macrophages depart from the site through lymph vessels. If these steps are strictly followed, then acute inammation resolves without tissue injury.
