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Related Concept Videos

Acute Inflammation I: Inflammatory Response01:26

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 ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
Inflammation01:38

Inflammation

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Related Experiment Video

Updated: Jul 7, 2026

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation
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A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

Published on: August 30, 2019

Anti-inflammatory and proresolving lipid mediators.

Charles N Serhan1, Stephanie Yacoubian, Rong Yang

  • 1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. cnserhan@zeus.bwh.harvard.edu

Annual Review of Pathology
|February 1, 2008
PubMed
Summary

Inflammation resolution involves active, proresolving lipid mediators like resolvins and protectins, not just passive healing. These omega-3 fatty acid derivatives offer potent anti-inflammatory and organ-protective effects.

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Facilitating Drug Discovery: An Automated High-content Inflammation Assay in Zebrafish
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A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation
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Area of Science:

  • Biochemistry
  • Immunology
  • Pharmacology

Background:

  • The traditional view linked lipid mediators primarily to inflammation, exemplified by prostaglandin synthesis inhibition by NSAIDs.
  • Inflammation resolution was historically considered a passive process.
  • Recent discoveries reveal active biochemical pathways and lipid mediators driving resolution.

Purpose of the Study:

  • To review recent advances in understanding the biosynthesis and actions of novel proresolving lipid mediators.
  • To highlight the identification of new mediator families from omega-3 polyunsaturated fatty acids.
  • To discuss the organ-protective and antifibrotic properties of these mediators.

Main Methods:

  • Utilized a lipid-mediator informatics approach to identify endogenous mediators in resolving inflammation.
  • Analyzed resolving exudates containing lipoxins, aspirin-triggered lipoxins, resolvins, and protectins.
  • Reviewed literature on the stereospecific actions and biosynthesis of these mediators.

Main Results:

  • Identified novel families of endogenous, locally acting mediators derived from omega-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid).
  • Characterized these new mediators as resolvins and protectins, possessing potent anti-inflammatory and proresolving actions.
  • Established that these mediators are actively involved in inflammation resolution and exhibit organ protection and antifibrotic effects.

Conclusions:

  • Inflammation resolution is an active, enzymatically controlled process involving specific lipid mediators.
  • Resolvins and protectins, derived from omega-3 fatty acids, are key players in promoting resolution and preventing tissue damage.
  • These findings challenge the traditional view and open new therapeutic avenues for inflammatory diseases.