Local inflammatory responses

Last updated: May 6, 2022

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Inflammation is the response of vascularized tissues to harmful stimuli such as infectious agents, mechanical damage, and chemical irritants. Inflammation has both local and systemic manifestations and can be either acute or chronic. Local inflammatory response (local inflammation) occurs within the area affected by the harmful stimulus. Acute local inflammation develops within minutes or hours following a harmful stimulus, has a short duration, and primarily involves the innate immune system. The five classic signs of acute local inflammation are redness, swelling, heat, pain, and loss of function. These signs are caused by the sequence of events that is triggered by tissue damage and allows leukocytes to reach the site of damage in order to eliminate the causative factor. This sequence involves changes in local hemodynamics and vessel permeability as well as interaction between leukocytes and endothelium and interstitial tissue, through which leukocytes escape the blood vessels. To sustain the vascular changes and attract more immune cells to the site of inflammation, leukocytes and tissue cells secrete a range of inflammatory mediators, including interleukins and chemokines. Elimination of the causative factor by leukocytes leads to the resolution of acute inflammation and tissue repair with complete regeneration or scarring. Failure to eliminate the causative agent or prolonged exposure to the causative agent leads to chronic inflammation, which confines the causative agent to the site of the initial acute inflammatory response. Chronic inflammation may last months to years and primarily involves the adaptive immune system.

Overview

  • Definition: an immediate response to a pathogenic factor (e.g., trauma, necrosis, foreign bodies, infection)
  • Characteristics

Involved components

Inflammatory reactions

  1. Local hemodynamic changes (vascular response to injury)
  2. Increased vascular permeability
  3. Cellular effects

Possible Outcomes

Possible outcomes of acute inflammation [3]
Outcome Description Associated mediators and cytokines
Persistent acute inflammation
Resolution with regeneration
Resolution with scarring
  • Cellular debris, pathogens, and edema are cleared.
  • There is a lack of stem cells to replace the damaged tissues
  • Original tissue is replaced by fibrotic scar tissue.
Abscess formation
  • Inflammation pus formation and tissue necrosis
  • The focus of necrosis is separated from healthy tissues by a fibrous capsule.
  • Septic abscess: an abscess that results from infection
  • Sterile abscess
    • An abscess that is not caused by infection
    • May form as a complication of subcutaneous/intramuscular injection when the injected substance (e.g., glucocorticoids, synthol, oils) is not absorbed and causes persistent irritation or as a result of ongoing inflammation in a previously septic abscess after the causative pathogen has been cleared.
Chronic inflammation
Signs of inflammation [3]
Sign Mechanism Mediators
Rubor (redness)
Calor (heat)
Tumor (swelling)
Dolor (pain)
Functio laesa (loss of function)
  • Caused by the combined effect of other cardinal signs (e.g., clenching of a fist is impossible because the hand has cellulitis)

General information

Margination

Rolling

Leukocyte adhesion

Selectins are molecules that allow leukocytes to select the place of their migration (weak binding), while integrins are molecules that integrate (strong binding) the leukocytes with the endothelial cells.

Diapedesis (transmigration)

Migration

Overview

Recognition [3]

Engulfment [3]

Killing and degradation [3]

Chronic inflammation may be preceded by acute inflammation and can last for months to years. [3]

Overview

Etiology

Pathophysiology

Pathology

TNF-α is important for maintaining the granuloma. It is essential to test patients for latent TB before initiating anti-TNF therapy because the drug causes breakdown of the granuloma and can result in disseminated TB.

References:[3][5][6]

  1. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2014
  2. Mariathasan S, Newton K, Monack DM, et al. Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf. Nature. 2004; 430 (6996): p.213-218. doi: 10.1038/nature02664 . | Open in Read by QxMD
  3. Broz P, Dixit VM. Inflammasomes: mechanism of assembly, regulation and signalling. Nature Reviews Immunology. 2016; 16 (7): p.407-420. doi: 10.1038/nri.2016.58 . | Open in Read by QxMD
  4. Granger DN, Senchenkova E.. Inflammation and the Microcirculation. Anatomical Considerations. 2010 : p.Chapter 3.
  5. Zhang H, Sun C, Glogauer M, Bokoch GM. Human Neutrophils Coordinate Chemotaxis by Differential Activation of Rac1 and Rac2. J Immunol. 2009; 183 (4): p.2718-2728. doi: 10.4049/jimmunol.0900849 . | Open in Read by QxMD
  6. McDonald B, Kubes P. Chemokines: sirens of neutrophil recruitment—but is it just one song?. Immunity. 2010; 33 (2): p.148-149. doi: 10.1016/j.immuni.2010.08.006 . | Open in Read by QxMD

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