Acute inflammation: vascular and cellular events !

Process

The quick local response to infection or injury: vessels widen and leak, and white cells leave the blood to reach the problem.

Updated 2026-11-01

What it is

Acute inflammation is a rapid, short-lived response that delivers fluid, plasma proteins and leukocytes, mainly neutrophils, to a site of infection or injury. Vascular changes (dilation and leakage) cause redness, heat and swelling, and mediators such as prostaglandins and bradykinin cause pain. It normally ends with clearance and repair; if the cause persists, it can become chronic.

Step by step

Brief arteriolar constriction, then vasodilation driven by histamine, prostaglandins and nitric oxide: redness and heat.
Endothelial cells contract and the venules leak protein-rich fluid (exudate): swelling.
Slower blood flow pushes leukocytes to the vessel wall (margination).
Rolling: selectins on endothelium and leukocytes make weak, transient contacts.
Firm adhesion: chemokines activate leukocyte integrins (LFA-1, Mac-1), which bind ICAM-1 on endothelium.
Transmigration (diapedesis) between endothelial cells, helped by PECAM-1.
Chemotaxis toward C5a, IL-8 (CXCL8), leukotriene B4 and bacterial peptides.
Neutrophils phagocytose and kill; macrophages arrive later, clear debris and start repair.

Mediators and what they cause

Mediator	Main source	Main effect
Histamine	Mast cells, basophils	Vasodilation and increased permeability (immediate)
Prostaglandins (PGE2, PGI2)	Arachidonic acid via cyclooxygenase	Vasodilation, pain, fever
Leukotriene B4	Arachidonic acid via lipoxygenase	Neutrophil chemotaxis
Leukotrienes C4, D4, E4	Mast cells, leukocytes	Bronchospasm and increased permeability
Bradykinin	Kinin system (plasma)	Permeability, vasodilation, pain
C3a and C5a	Complement	Mast cell degranulation; C5a attracts neutrophils
TNF and IL-1	Macrophages	Endothelial activation, fever, acute-phase response

Clinical notes

The cardinal signs are redness, heat, swelling, pain and loss of function.
Leukocyte adhesion deficiency type 1 (CD18 integrin defect): delayed separation of the umbilical cord, infections without pus and marked neutrophilia.
NSAIDs block cyclooxygenase and therefore reduce prostaglandin-mediated pain and fever.
Glucocorticoids raise the circulating neutrophil count partly by reducing their adhesion to vessel walls (demargination).

Test yourself

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

Which molecules mediate leukocyte rolling, and which mediate firm adhesion?

Rolling depends on selectins (E-, P- and L-selectin); firm adhesion depends on leukocyte integrins such as LFA-1 binding ICAM-1 on endothelium.

A newborn has delayed umbilical cord separation and infections without pus. Which defect is likely?

Leukocyte adhesion deficiency type 1, a defect in the CD18 integrin chain that prevents neutrophils from leaving vessels.

Which three molecules are classic neutrophil chemoattractants?

C5a, IL-8 (CXCL8) and leukotriene B4; bacterial formyl peptides also attract neutrophils.

Which cell type predominates in the first one to two days of acute inflammation?

The neutrophil; macrophages become more prominent afterward.

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In Pharmacology

Nonsteroidal anti-inflammatory drugs (NSAIDs)

← All of immunology

Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.

Sources: 17.5 Inflammation and Fever (OpenStax (Microbiology), 2016); 21.2 Barrier Defenses and the Innate Immune Response (OpenStax (Anatomy and Physiology 2e), 2022).

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Representative model, for educational purposes only.