Inflammation: Acute


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.


Bertheloot D and Latz E (2017) HMGB‐1, IL1α, IL‐33 and S100 proteins dual‐function alarmins. Cellular and molecular immunology 14: 43–64.

Bottazzi B, Doni A, Garlanda C and Mantovani A (2010) An integrated view of Humoral immunity: pentraxins as a paradigm. Annual Review of Immunology 28: 157–183.

Dey A, Allen J and Hankey‐Giblin PA (2015) Ontogeny and polarisation of macrophages in inflammation; blood monocytes versus tissues macrophages. Frontiers in Immunology 5: 683.

DiPietro LA (2016) Angiogenesis and wound repair: when enough is enough. Journal of Leukocyte Biology. 5: 979–984.

Filippi MD (2016) Mechanism of diapedesis; importance of the transcellular route. Advances in Immunology 129: 25–53.

Fullerton JN and Gilroy DW (2016) Resolution of inflammation: a new therapeutic frontier. Nature Reviews. Drug Discovery 15: 551–567.

Griffith JW, Sokol CL and Luster AD (2014) Chemokines and chemokine receptors: positioning cells for host defence and immunity. Annual Review of Immunology 32: 659–702.

Margetic S (2012) Inflammation and haemostasis. Biochemia Medica 22: 49–62.

Medzhitov R and Hornung T (2009) Transcriptional control of the inflammatory response. Nature Reviews. Immunology 9: 692–703.

Rivera A, Siracusa MC, Yap GS and Gause WC (2016) Innate cell communication kick starts pathogen‐specific immunity. Nature Immunology 17: 356–363.

Sharma A and Kannegantu TD (2016) The cell‐biology of Inflammasomes: mechanisms of assembly regulation and signalling. Journal of Cell Biology 213: 617–629.

Takeuchi O and Akira S (2010) Pattern recognition receptors and inflammation. Cell 140 (6): 805–820.

Tan SY and Weninger W (2016) Neutrophil migration in inflammation; intercellular signal relay and crosstalk. Current Opinion in Immunology 44: 34–42.

Ward‐Kavanagh LK, Lin WW, Sedy JR and Ware CF (2016) The TNF receptor superfamily in co‐stimulating and co‐inhibitory responses. Immunity 44: 1005–1019.

Wynn TA and Vannella KM (2016) Macrophages in tissue repair, regeneration and fibrosis. Immunity 44: 450–462.

Further Reading

Matzinger P (2007) Friendly and dangerous signals: is the tissue in control? Nature Immunology 8: 11–13.

Serhan CN, Ward PA and Gilroy DW (2010) Fundementals of Inflammation. Cambridge, UK: Cambridge University Press.

Contact Editor close
Submit a note to the editor about this article by filling in the form below.

* Required Field

How to Cite close
Raynes, John G(Jun 2017) Inflammation: Acute. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0000943.pub3]