Inflammation: the cardinal signs and its five steps !

Topic

Inflammation is how living tissue answers injury or infection: it brings blood, fluid and white cells to the spot, cleans up, then repairs.

Updated 2026-11-01

What it is

Inflammation is the response of vascularised tissue to infection or damage. It brings plasma proteins and leukocytes from the blood to the injured site to destroy the cause, clear dead tissue and start repair. It is protective, but when it is too strong, aimed at the wrong target or never switched off, it becomes the disease itself, from anaphylaxis to rheumatoid arthritis and atherosclerosis.

Step by step

Recognition: sentinel cells (macrophages, dendritic cells, mast cells) detect microbes or dead-cell products through receptors such as Toll-like receptors.
Sensors such as the inflammasome trigger the release of IL-1, TNF, histamine, prostaglandins and chemokines.
Recruitment: arterioles dilate, venules leak, and neutrophils roll, stick and squeeze out toward the site.
Removal: leukocytes engulf and kill the microbes and clear necrotic debris.
Regulation: short-lived mediators decay and anti-inflammatory signals (IL-10, TGF-β, lipoxins) switch the response off.
Resolution and repair: fluid drains through lymphatics; tissue regenerates or is replaced by a scar.

Acute vs chronic inflammation

Feature	Acute	Chronic
Onset and duration	Fast (minutes to hours); lasts days	Slow (days to weeks); lasts months or years
Main cells	Neutrophils	Macrophages, lymphocytes, plasma cells
Vascular changes	Marked vasodilation and oedema	Less oedema; growth of new vessels (angiogenesis)
Tissue damage	Usually mild and self-limited	Often progressive, with fibrosis
Local and systemic signs	Prominent: redness, heat, pain, fever	Subtler; may be silent for years
Typical example	Acute appendicitis	Rheumatoid arthritis, tuberculosis

Clinical notes

Anti-inflammatory drugs act on specific steps of this sequence: NSAIDs on prostaglandins, glucocorticoids on many genes, biologics on TNF or IL-6.
Inflammation that fails to switch off underlies many chronic diseases: rheumatoid arthritis, inflammatory bowel disease, atherosclerosis.
People who cannot mount inflammation (severe neutropenia, long-term glucocorticoids) may have serious infections with few local signs.

Test yourself

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

Which vascular change explains the redness and heat of inflammation?

Arteriolar dilation, mainly from histamine, nitric oxide and prostaglandins, which increases blood flow to the area.

Which leukocyte predominates on the first day of acute inflammation, and which replaces it?

Neutrophils in the first 6–24 hours; monocytes, which become macrophages, by 24–48 hours.

When does inflammation become harmful rather than protective?

When it is excessive, aimed at the body's own tissues or harmless antigens, or does not stop, as in autoimmune disease, allergy and chronic infection.

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: 17.5 Inflammation and Fever (OpenStax (Microbiology), 2016); 4.6 Tissue Injury and Aging (OpenStax (Anatomy and Physiology 2e), 2022); Appendicitis (StatPearls (NCBI Bookshelf), 2024).

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Representative model, for educational purposes only.