Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.

Recognition and Mediator Release

The inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns (PAMPs) via pattern recognition receptors (PRRs). Activation of these cells leads to the secretion of inflammatory mediators, including histamine, prostaglandins, leukotrienes, and pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α).

Vascular Changes

Histamine and prostaglandins cause vasodilation of local arterioles, increasing blood flow and resulting in erythema and heat. Simultaneously, vascular permeability increases, allowing plasma proteins and fluids to move into the interstitial space, contributing to localized edema. These vascular changes facilitate the delivery of immune components to the site of injury.

Leukocyte Recruitment

Leukotrienes act as potent chemoattractants, guiding neutrophils and other immune cells toward the inflamed tissue. Cytokines such as IL-1 and TNF-α activate endothelial cells to express adhesion molecules, promoting the tethering and rolling of leukocytes along the vascular endothelium. Reduced flow velocity due to plasma leakage facilitates the firm adhesion and transmigration of neutrophils across the endothelium through diapedesis.

Effector Functions

Once in the tissue, neutrophils perform critical effector functions, including the phagocytosis of pathogens, the release of antimicrobial enzymes, and the clearance of necrotic debris. These actions contribute to the resolution of inflammation and the initiation of tissue repair.