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Physiology · Blood, hemostasis and basic immunity

The physiology of inflammation !

  • Mechanism
  • Exam priority: medium

Inflammation is the body's alarm: vessels widen and leak so defence cells and proteins reach the injury. That is why it gets red, hot, swollen and sore.

Updated 2026-11-01

Also called: Acute inflammation, Acute phase response

See it in 3D: Liver · Hypothalamus

What it is

Inflammation is the coordinated vascular and cellular response to infection or tissue damage. Sentinel cells detect danger signals and release mediators that dilate arterioles, make venules leaky and call in leukocytes. When the cause is removed, active resolution follows; if not, inflammation becomes chronic and damages the tissue it protects.

How it works, step by step

  1. Microbes (PAMPs) or damaged cells (DAMPs) are detected by receptors such as Toll-like receptors on macrophages and mast cells.
  2. Mast cells release histamine within seconds → arteriolar dilation and endothelial gaps in postcapillary venules.
  3. Macrophages release IL-1, TNF-α and chemokines; arachidonic acid becomes prostaglandins and leukotrienes.
  4. More flow (redness, heat) and leaky venules let plasma proteins out → oncotic gradient falls → swelling.
  5. Endothelium expresses selectins and ICAM-1 → neutrophils roll, stick and cross into the tissue toward chemokines.
  6. Neutrophils phagocytose and kill with oxidants and enzymes; complement (C3b) coats targets and C5a attracts more cells.
  7. Bradykinin and PGE₂ sensitize nociceptors → pain and tenderness protect the injured part.
  8. Resolution: lipoxins and resolvins stop recruitment, macrophages clear dead neutrophils, and repair begins.

Regulation

  • +Histamine, bradykinin: Vasodilation and increased permeability
  • +IL-1, TNF-α, IL-6: Endothelial activation, fever, acute-phase response
  • +Complement C3a/C5a, leukotriene B₄, IL-8: Recruit and activate neutrophils
  • −Cortisol: Suppresses cytokine and eicosanoid synthesis
  • −IL-10, TGF-β, lipoxins and resolvins: Switch off recruitment and promote repair

Clinical notes

  • C-reactive protein rises within 6–8 h and falls quickly when inflammation ends; the ESR rises more slowly because it depends on fibrinogen.
  • Sepsis is inflammation that escapes local control: diffuse vasodilation and capillary leak cause hypotension and organ failure.
  • Rheumatoid arthritis is chronic inflammation: persistent cytokine production (TNF-α, IL-6) erodes cartilage and bone.

Test yourself

Think of the answer, then tap the question to see it.

Why does an inflamed area swell?

Mediators open gaps between venular endothelial cells; proteins leak out, lowering the plasma–tissue oncotic gradient, and fluid follows into the interstitium as a protein-rich exudate.

How does a local infection produce fever?

IL-1, TNF-α and IL-6 reach the hypothalamus and induce COX-2 to make PGE₂, which raises the temperature set point; the body then conserves and generates heat.

Why is CRP useful for following acute inflammation?

IL-6 drives hepatic CRP synthesis within hours and CRP has a short half-life, so levels rise and fall closely with inflammatory activity.

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The structures of Durgical's 3D anatomy where it happens.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 21.2 Barrier Defenses and the Innate Immune Response (OpenStax (Rice University), 2022); 18.4 Leukocytes and Platelets (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 34). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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