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Acute inflammation — vascular changes, leukocyte recruitment and mediators
Acute inflammation is a rapid response of blood vessels and white cells to injury or infection: vasodilation and increased permeability bring fluid and protein into tissue, and neutrophils adhere to endothelium, cross it and destroy the agent — mediated by histamine, prostaglandins, leukotrienes, cytokines and complement.
Why it matters in the exam
The bank tests defined steps and molecules. The steps of leukocyte recruitment: rolling mediated by selectins — E-selectin and P-selectin on endothelium; firm adhesion mediated by leukocyte integrins (LFA-1, Mac-1) binding ICAM-1; migration between endothelial cells (diapedesis) mediated by PECAM-1 (CD31), which is also an immunohistochemical endothelial marker; and chemotaxis towards C5a, leukotriene B4, IL-8 and bacterial products. Integrin deficiency (LAD) causes recurrent infections without pus.
Increased permeability results mainly from endothelial contraction in post-capillary venules in response to histamine and bradykinin; bradykinin also causes pain and vasodilation. Histamine is released from mast cells by IgE cross-linking, by complement anaphylatoxins (C3a, C5a) and by physical stimuli. Prostaglandin E2 causes pain and fever, prostacyclin vasodilation, and thromboxane A2 vasoconstriction and platelet aggregation. IL-1 and TNF cause fever via hypothalamic PGE2 and hepatic production of acute-phase proteins — CRP, serum amyloid A, fibrinogen and hepcidin; albumin falls in inflammation and is therefore not a positive acute-phase protein.
Bacterial killing in phagocytes is done mainly by the myeloperoxidase–hydrogen peroxide–halide system, which produces hypochlorite, and is the most efficient; NADPH oxidase produces the initial radicals, and its deficiency causes chronic granulomatous disease. The morphological patterns: serous, fibrinous (for example the pericardium), purulent (from pyogenic bacteria such as staphylococci and streptococci) and ulcer. Outcomes: complete resolution, abscess, scar or progression to chronic inflammation. Neutrophils predominate in the first 6–24 hours, and macrophages after 24–48 hours.
Key points
- Rolling by selectins, adhesion by integrins, transmigration by PECAM-1.
- Increased permeability from histamine and bradykinin in venules.
- PGE2 for pain and fever; IL-1 and TNF for the systemic response.
- Bacterial killing: myeloperoxidase and hydrogen peroxide.
- Acute-phase proteins: CRP, serum amyloid A, fibrinogen, hepcidin; not albumin.
Summary table
| Step or mediator | Main molecule | Effect | Pitfall |
|---|---|---|---|
| Rolling | E-selectin and P-selectin | Slowing of leukocytes | Confusing with integrins |
| Firm adhesion | LFA-1 and Mac-1 with ICAM-1 | Arrest on endothelium | Deficiency — LAD without pus |
| Transmigration | PECAM-1 (CD31) | Exit into tissue | Thinking it is a selectin |
| Increased permeability | Histamine, bradykinin | Protein-rich oedema | Thinking bradykinin only constricts |
| Fever and acute-phase proteins | IL-1, TNF, IL-6; CRP and fibrinogen | Systemic response | Listing albumin as acute-phase |
A free exam question
איזה מבין הבאים הוא מקור להיסטמין )histamine ( בתגובה הדלקתית? (the question as examined, in Hebrew)
- א. Hepatocyte
- ב. Lymphocyte
- ג. Neutrophil
- ד. Platelet
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Sources
- Robbins and Cotran Pathologic Basis of Disease, 10th edition (2021) — Inflammation and repair — acute inflammation
- Abbas AK, Lichtman AH, Pillai S. Cellular and Molecular Immunology, 10th edition (2022) — Innate immunity and leukocyte migration
- Rubin's Pathology: Mechanisms of Human Disease, 8th edition (2020) — Inflammation
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.