General pathology · Inflammation
Mediators of inflammation: the table to know !
- Topic
Inflammation is run by chemical messengers from cells and plasma; knowing who makes each one and what it does explains the signs and the drugs.
Updated 2026-11-01
What it is
Mediators are the signals that start, amplify and stop inflammation. Some are stored in cells and released in seconds (histamine), some are made on demand (prostaglandins, leukotrienes, cytokines), and some circulate as inactive plasma precursors activated by cleavage (complement, kinins, clotting factors). Most act briefly and locally, and their actions overlap, so blocking one rarely stops the whole response.
Key facts
- Preformed: histamine, serotonin, lysosomal enzymes. Made on demand: prostaglandins, leukotrienes, PAF, cytokines, nitric oxide, reactive oxygen species.
- Plasma-derived mediators (complement, kinins, clotting proteins) are made mainly in the liver and circulate inactive until cleaved.
- Most mediators have short half-lives, are quickly degraded or inhibited, and act through specific receptors.
- One mediator can trigger others (TNF and IL-1 induce chemokines and prostaglandins), which amplifies the response.
Main mediators and their actions
| Mediator | Main source | Main actions |
|---|---|---|
| Histamine | Mast cells, basophils, platelets (preformed) | Arteriolar dilation, venular leakage, bronchoconstriction |
| Serotonin | Platelets, enterochromaffin cells | Mainly vasoconstriction; small role in human inflammation |
| Prostaglandins (PGE2, PGI2, PGD2) | Mast cells, leukocytes, endothelium (from arachidonic acid) | Vasodilation, pain, fever (PGE2) |
| Thromboxane A2 | Platelets | Vasoconstriction, platelet aggregation |
| Leukotriene B4 | Neutrophils, macrophages | Neutrophil chemotaxis and activation |
| Leukotrienes C4, D4, E4 | Mast cells, eosinophils | Bronchospasm, venular leakage, vasoconstriction |
| Platelet-activating factor (PAF) | Leukocytes, endothelium, platelets | Platelet aggregation, leakage, bronchoconstriction, leukocyte adhesion |
| TNF and IL-1 | Macrophages, mast cells, endothelium | Endothelial activation (adhesion molecules), fever, acute-phase response, sepsis |
| IL-6 | Macrophages and other cells | Acute-phase proteins from the liver (CRP, fibrinogen, hepcidin) |
| Chemokines (IL-8 = CXCL8) | Macrophages, endothelium | Neutrophil chemotaxis and integrin activation |
| C3a, C5a | Complement cleavage | Mast cell degranulation (anaphylatoxins); C5a is a strong chemoattractant |
| C3b; C5b-9 | Complement cleavage | Opsonisation; the membrane attack complex lyses microbes |
| Bradykinin | Kinin system (high-molecular-weight kininogen) | Leakage, vasodilation, smooth muscle contraction, pain |
| Nitric oxide | Endothelium, macrophages | Vasodilation; microbial killing in macrophages |
| Reactive oxygen species, lysosomal enzymes | Neutrophils, macrophages | Microbial killing; tissue injury when released |
Clinical notes
- Drugs block one arm at a time: antihistamines (H1), NSAIDs (cyclooxygenase), leukotriene receptor antagonists, anti-TNF and anti-IL-6 antibodies, IL-1 blockers.
- IL-1 blockers work in autoinflammatory diseases such as familial Mediterranean fever, in which the inflammasome is overactive.
Test yourself
Think of the answer, then tap the question to see it.
Which mediators cause pain in inflammation?
Mainly prostaglandin E2 and bradykinin, which sensitise and stimulate sensory nerve endings.
Which complement fragments act as anaphylatoxins, and which one is also chemotactic?
C3a and C5a trigger mast cell degranulation; C5a is also a potent chemoattractant for neutrophils.
Which cytokines produce fever and the acute-phase response?
IL-1, TNF and IL-6; IL-6 is the main driver of acute-phase protein synthesis in the liver.
Related
- Arachidonic acid metabolites in inflammation, and the drugs that block them
- Histamine, serotonin, bradykinin and the plasma protein cascades
- Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate
- Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxis
- Systemic effects of inflammation: fever, acute-phase proteins, leukocytosis, sepsis
- When leukocytes injure tissue: proteases, oxidants and NETs
Related conditions
- Anaphylaxis
- Urticaria and angioedema
- Asthma
- Sepsis and septic shock
- Rheumatoid arthritis
- Gout
- Carcinoid syndrome
- Familial Mediterranean fever and other hereditary autoinflammatory syndromes
Elsewhere in DurgiPedia
- Eicosanoids: prostaglandins, thromboxanes and leukotrienes
- Cytokines: the table to know
- Complement: three pathways, MAC, regulators
- TNF-α
- Interleukin-1
- Interleukin-6
- IL-8 and the chemokines
- Nitric oxide (NO)
- Mast cell and basophil
In Pharmacology
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); Hereditary angioedema: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); Pain Relievers | Analgesics | Painkillers | MedlinePlus (MedlinePlus, US National Library of Medicine, 2026).
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Representative model, for educational purposes only.