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Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: Local and Systemic Effects

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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...
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Chronic Inflammation: Introduction01:12

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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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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.
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Acute Inflammation I: Inflammatory Response01:26

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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...
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Fats and lipids are crucial components in the human body. Some lipid-derived compounds, such as fat-soluble vitamins, eicosanoids, lipoproteins, and glycolipids, also play unique roles to support various  biological processes .
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Acute Inflammation I: Cellular Phase01:26

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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...
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Related Experiment Video

Updated: May 5, 2026

Methods to Study Lipid Alterations in Neutrophils and the Subsequent Formation of Neutrophil Extracellular Traps
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Lipid mediators in immune dysfunction after severe inflammation.

James N Fullerton1, Alastair J O'Brien1, Derek W Gilroy1

  • 1Centre for Clinical Pharmacology, Division of Medicine, Rayne Institute, 5 University Street, University College London, London, WC1E 6JF, UK.

Trends in Immunology
|November 26, 2013
PubMed
Summary
This summary is machine-generated.

Critical illness involves immune system defects and altered lipid mediators. Targeting these bioactive lipid mediators offers potential therapeutic strategies for critical illness treatment.

Keywords:
cyclooxygenaseeicosanoidsimmunosuppressionprostaglandinsresolution of inflammationsepsis

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Area of Science:

  • Immunology
  • Biochemistry
  • Critical Care Medicine

Background:

  • Major trauma, sepsis, burns, and surgery trigger systemic inflammation.
  • Immune dysfunction in critical illness is linked to altered leukocyte gene expression and impaired immune cell function.
  • Impaired resolution of inflammation, involving bioactive lipid mediators, contributes to critical illness pathology.

Purpose of the Study:

  • To reassess the therapeutic potential of manipulating bioactive lipid mediators (LMs) in critical illness.
  • To explore pharmacological strategies targeting inflammatory and proresolving LMs.

Main Methods:

  • Review of recent data on immune responses in critical illness.
  • Analysis of the role of prostaglandins and specialized proresolving LMs.
  • Assessment of potential pharmacological interventions targeting LMs.

Main Results:

  • Critical illness involves a distinct, prolonged leukocyte transcriptome response.
  • Defects in innate and adaptive immunity are observed.
  • Dysregulation of inflammatory resolution pathways and LMs are key contributors.

Conclusions:

  • Pharmacological manipulation of bioactive lipid mediators presents a promising therapeutic avenue for critical illness.
  • Targeting prostaglandins or specialized proresolving LMs may offer new treatment strategies.