Epithelial injury cellular events

Only few detailed analyses of the intracellular events following epithelial injury have been performed using cells from the airways, and most mechanistic work has concentrated on pre-necrotic and necrotic processes in epitheUal cells of renal origin (Trump etal., 1980, 1981 Trump and Berezesky, 1984). Collectively these studies, which have employed a wide range of stimuli to evoke cellular injury (ischaemia, metabolic poisons, chaotropic agents and ionophores), suggest that similar patterns of intracellular events accompany injury evoked by the different stimuli. 

Inflammatory mediators released at the site of an injury stimulate a cascade of events necessary for the repair and resolution of injury. A number of cells participate in the inflammatory response, including monocytes/ macrophages, neutrophils, and lymphocytes. Structural cells such as fibroblasts and epithelial cells also play critical roles in directing the inflammatory response. Cellular injury results in the release of reactive oxygen species, arachadonic-acid metabolites, inflammatory cytokines, and chemokines that generate an inflammatory response. These paracrine mediators orchestrate complex interactions between the surrounding cell populations and direct the inflammatory responses necessary to restore homeostasis. The chemokine family members appear to play a particularly important role in directing the movement and localization of immune and inflammatory cells. 

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