U01.04.014 Acute inflammation

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Learning Objectives

Define the characteristics of Acute Inflammation and identify the primary triggers of the innate immune response. Master the vascular and cellular components of the inflammatory process, and understand the role of the Inflammasome in activating IL-1.

1. Characteristics and Stimuli

Acute inflammation is a transient, early response (seconds to days) characterized by the presence of neutrophils and edema. It is a non-specific reaction of the innate immune system to external or internal insults.

Category Examples / Details
Stimuli Infections (bacteria/virus), trauma, tissue necrosis, and foreign bodies.
Mediators Toll-like receptors, Arachidonic acid metabolites, Complement, Hageman factor (XII).
The Inflammasome Protein complex recognizing uric acid crystals/dead cells → Activates IL-1.

 

2. The Two Major Components

The goal of acute inflammation is to deliver cells (WBCs) and proteins (antibodies/complement) to the site of injury via two coordinated shifts:

Component Mechanism Outcome
Vascular Vasodilation and ↑ endothelial permeability (contraction). Stasis and protein-rich fluid leakage (edema).
Cellular Extravasation from postcapillary venules. Neutrophil accumulation and activation at the injury site.

3. Outcomes of Acute Inflammation

The transition from acute inflammation to resolution or chronicity is determined by the specific cytokines released, particularly by macrophages, which peak 2–3 days after onset.

Outcome Mediators / Features
Resolution & Healing Driven by anti-inflammatory IL-10 and TGF- \beta.
Abscess Acute inflammation is walled off by fibrosis.
Chronic Inflammation Macrophage antigen presentation activates CD4+ T cells.
Persistent Acute Maintained by IL-8 (neutrophil chemotaxis).

 

Activity

High-Yield Mnemonics & Tips:

  • Neutrophil Timing: Neutrophils are the first responders (Acute). If you see Macrophages dominating, you are likely 2–3 days into the process or transitioning to chronic.
  • IL-8: Remember “Clean up on aisle 8.” IL-8 is the primary cytokine that keeps neutrophils coming to the site.
  • Hageman Factor (XII): Links subendothelial collagen damage to clotting, fibrinolysis, and the kinin system (pain/vasodilation).

Activity: