Inflammation represents the response of vascularised tissue to damage resulting from infection or injury. An acute inflammatory response comprises four phases: detection of harmful stimuli, recruitment of effector molecules and cells, elimination of pathogens and cellular debris and restoration of tissue homeostasis. Several receptor families, including Toll-like receptors, Nod-like receptors and C-type lectins, recognise molecules associated with microbial pathogens and cellular damage. Signals mediated by these receptors stimulate the release of inflammatory molecules that alter vascular permeability at sites of tissue damage. Changes in vascular endothelium promote the exudation of plasma and the recruitment of leucocytes for the clearance of microorganisms and necrotic tissue. Inflammatory mediators also exert systemic effects that contribute to immune defence in a process called the acute-phase response. Successful clearance of injurious agents and tissue damage abates inflammatory signals and is followed by the formation of granulation tissue and the initiation of tissue remodelling.

Key Concepts:

• Tissues are continuously surveyed for infection and cellular damage by cells and molecules that recognise pathogen- and damage-associated molecular patterns.
  
• Recognition of infection or cellular damage activates inflammation locally and systemically to eliminate microbial pathogens and damaged tissue.
  
• Inflammatory signals recruit neutrophils and macrophages into inflamed tissues where they release toxic factors and phagocytose pathogens and cellular debris.
  
• The resolution of inflammation is followed by tissue repair and remodelling.