Inflammation: Acute

Abstract

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, response from effector molecules and cells, elimination of pathogens and cellular debris and restoration of tissue homeostasis. Innate pattern recognition molecules are found in extracellular, cell surface and intracellular locations and bind to components of microbes or molecules released by cellular damage. These trigger pathways that lead to the release of inflammatory molecules that alter vascular permeability at sites of tissue damage and activation of many immune cells. Changes in vascular endothelium promote the exudation of plasma and leucocyte recruitment for the clearance of microorganisms and necrotic tissue. Inflammatory mediators also exert systemic effects 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 activate immune cells and 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.
  • Inflammation has many feedback control mechanisms because if unrestrained it can lead to severe pathology.
  • The resolution of inflammation is followed by tissue repair and remodelling.

Keywords: coagulation; platelets; leucocytes; phagocytosis; wound healing; cytokines; neutrophils; macrophages; acute‐phase response

Figure 1. Stages of the acute inflammatory response. (a) The inflammatory process begins with vascular coagulation (clotting) and the detection of pathogens or cellular injury by pattern recognition receptors (PRR). (b) Signalling through PRR induces inflammatory mediators which act on blood vessels to promote the recruitment of leucocytes and exudation of plasma into the damaged tissue. (c) After elimination of microorganisms and necrotic tissue, leucocyte recruitment ceases and apoptotic neutrophils are phagocytosed by macrophages. (d) Tissue repair and remodelling involves the development of new blood vessels (angiogenesis), resurfacing of the wound (re‐epithelialisation) and collagen deposition.
Figure 2. Clot formation. Tissue injury results in fibrin formation to form the blood clot, which stops the bleeding and provides the scaffolding on which platelets aggregate and release mediators. The mediators influence vascular permeability and attract leucocytes from the blood. L, lymphocyte; M, macrophage and N, neutrophil. Illustration by Jeffrey Aarons.
Figure 3. Leucocyte adhesion and recruitment. At a site of inflammation, activated vascular endothelial cells express adhesion receptors which bind leucocytes that bear the matching adhesion molecules. This initially slows the leucocytes down, allowing them to sense the environment and then to attach more firmly and migrate between the endothelial cells to the inflamed tissue. N, neutrophil; M, macrophage; L, lymphocyte and VCAM, vascular cell adhesion molecule. Illustration by Jeffrey Aarons.
Figure 4. Phagocytosis. Once in the inflamed tissue, neutrophils and macrophages take up tissue debris and microorganisms. Bacteria are rapidly recognised if they are opsonised (coated by antibodies or complement) by the Fc and C3 receptors. Pseudopodia wrap around the attached particle and engulf it into a phagocytic vacuole. Lysosomes, which contain microbicidal enzymes, fuse with the phagocytic vacuole to form a phagolysosome, where the particles are digested. Illustration by Jeffrey Aarons.
Figure 5. Healing and scar formation. As the inflammation is resolved, leucocytes, especially macrophages (M), release growth factors which stimulate fibroblasts to divide and to make new extracellular matrix (scar) to heal injured tissue. FGF, fibroblast growth factor; PDGF, platelet‐derived growth factor and TGFβ, transforming growth factor β. Illustration by Jeffrey Aarons.
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How to Cite close
Raynes, John G(Jun 2017) Inflammation: Acute. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0000943.pub3]