Resolution of acute inflammation

Resolution of acute inflammation

Resolution of acute inflammation

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Outcomes of Acute Inflammation - The Aftermath

  • Complete Resolution: Ideal outcome with restoration of normal tissue architecture. Occurs with minimal damage and high regenerative capacity.
  • Healing by Fibrosis (Scarring): Occurs after substantial tissue destruction or in non-regenerative tissues.
  • Abscess Formation: A walled-off collection of pus (neutrophils & necrotic debris), typical of pyogenic bacterial infections.
  • Progression to Chronic Inflammation: Results from persistent injurious stimuli or interference with normal healing.

⭐ Resolution is an active process mediated by specialized pro-resolving mediators (SPMs) like lipoxins, resolvins, and protectins.

Resolution's Key Players - The Clean-Up Crew

  • Macrophages (M2 Phenotype): The primary "clean-up" cells.

    • Phagocytose apoptotic neutrophils & cellular debris.
    • Secrete anti-inflammatory cytokines (e.g., TGF-β, IL-10).
    • Produce growth factors to initiate tissue repair.
  • Specialized Pro-Resolving Mediators (SPMs): Actively terminate inflammation.

    • Lipoxins: Generated via neutrophil-platelet interaction.
    • Resolvins & Protectins: Derived from omega-3 fatty acids (EPA, DHA).
    • Function: Inhibit neutrophil chemotaxis & adhesion; stimulate clearance of apoptotic cells.

Resolution of Acute Inflammation and Tissue Repair

Macrophage Polarization: The switch from pro-inflammatory M1 macrophages to anti-inflammatory M2 macrophages is a critical step for inflammation to resolve and transition into a healing phase. This switch is driven by phagocytosis of apoptotic cells and cytokines like IL-4 and IL-13.

Mechanisms of Resolution - Winding It Down

  • Active Termination: Resolution is an active, programmed process, not just a passive decay of the inflammatory response.
  • Lipid Mediator Class Switch: A pivotal shift occurs from pro-inflammatory leukotrienes to anti-inflammatory lipoxins.
    • This switch is initiated by neutrophils, which then undergo apoptosis.
  • Specialized Pro-Resolving Mediators (SPMs):
    • Includes Resolvins, Protectins, and Maresins, derived from omega-3 fatty acids.
    • These molecules halt neutrophil influx and promote the clearance of apoptotic cells (efferocytosis).
  • Cytokine Profile Change: Shift towards anti-inflammatory cytokines, primarily IL-10 and TGF-β.

⭐ The "lipid mediator class switch" is a core principle. Aspirin-triggered lipoxins are a key pharmacologic example, enhancing resolution by mimicking this natural pathway.

Failed Resolution - The Lingering Problem

  • Failure of acute inflammation to resolve leads to:
    • Abscess Formation: A collection of pus (neutrophils, necrotic debris) confined by a fibrous capsule. Typically caused by pyogenic organisms like S. aureus. Liver abscess with fibrous capsule and necrotic center
    • Chronic Inflammation: Develops if the injurious agent persists, marked by an influx of lymphocytes and macrophages.
    • Fibrosis (Scarring): Tissue replacement with collagen following substantial destruction, a process termed "organization," resulting in functional loss.

⭐ The abscess capsule is produced by fibroblasts, a key feature distinguishing it from diffuse purulent inflammation (cellulitis).

High‑Yield Points - ⚡ Biggest Takeaways

  • Complete resolution is the ideal outcome, where macrophages clear debris and restore normal tissue structure.
  • Fibrosis (scarring) results from substantial tissue destruction or in non-regenerating tissues, mediated by fibroblasts.
  • Abscess formation (pus) is characteristic of pyogenic bacterial infections, like Staphylococcus aureus.
  • Progression to chronic inflammation occurs when the injurious agent persists, involving lymphocytes and macrophages.
  • Key anti-inflammatory mediators driving resolution include lipoxins, resolvins, and cytokines like IL-10 and TGF-β.

Practice Questions: Resolution of acute inflammation

Test your understanding with these related questions

A researcher is studying the interactions between foreign antigens and human immune cells. She has isolated a line of lymphocytes that is known to bind antigen-presenting cells. From this cell line, she has isolated a cell surface protein that binds to class I major histocompatibility complex molecules. The continued activation, proliferation and survival of this specific cell line requires which of the following signaling molecules?

1 of 5

Flashcards: Resolution of acute inflammation

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Are acute phase reactants produced by liver in acute or chronic inflammatory states?_____

TAP TO REVEAL ANSWER

Are acute phase reactants produced by liver in acute or chronic inflammatory states?_____

Both

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