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[Contribution of cytokines to inflammatory mechanisms].
- Source :
-
Pathologie-biologie [Pathol Biol (Paris)] 1993 Oct; Vol. 41 (8 Pt 2), pp. 799-811. - Publication Year :
- 1993
-
Abstract
- A large number of cytokines are found within foci of inflammation. Two of these cytokines, namely interleukin-1 (IL-1) and tumor necrosis factor (TNF), play a key role in orchestrating the mechanisms responsible for inflammation. These two cytokines induce production by many cells of lipid mediators, proteases, and free radicals, all of which play a direct role in development of the deleterious effects of inflammation. IL-1 and/or TNF exert cytotoxic effects on the vascular endothelium, cartilage, bone, muscle, or pancreatic beta-cell islets. Cytokines, including interferon gamma (IFN), IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF), amplify the inflammatory response by increasing production of IL-1 and TNF by macrophages. Macrophages also produce other cytokines, such as IL-8 and macrophage chemoattractant protein-1 (MCP-1), with chemoattractant properties that contribute to draw leucocytes to the site of inflammation. IL-6, produced in large amounts during inflammatory processes, induces the production of acute phase proteins by hepatocytes. IL-1, TNF, IL-11, leukemia inhibitory factor (LIF), and transforming growth factor beta (TGF beta) share this effect. TGF beta also has a number of anti-inflammatory effects. TGF beta, IL-4, and IL-10 inhibit production of IL-1 and TNF. Glucocorticoids also have this effect. Glucocorticoids can be produced as a result of a chain of events initiated by IL-1, TNF, and IL-6 and involving the neuro-endocrine axis. Other substances, such as IL-1 receptor antagonist (IL-1 ra) or soluble forms of the TNF receptors, can specifically inhibit the effects of IL-1 and TNF. Cascade production of cytokines, inhibition, negative feed-back, and synergistic mechanisms are parameters that illustrate the concept of "cytokine network" and aptly characterize the role of these mediators in the mechanisms of inflammation.
- Subjects :
- Acute-Phase Proteins biosynthesis
Blood Coagulation drug effects
Central Nervous System drug effects
Cytokines adverse effects
Cytokines metabolism
Endopeptidases biosynthesis
Endothelium, Vascular drug effects
Free Radicals metabolism
Humans
Inflammation metabolism
Inflammation physiopathology
Interleukin-1 adverse effects
Interleukin-1 metabolism
Prostaglandins biosynthesis
Tumor Necrosis Factor-alpha adverse effects
Tumor Necrosis Factor-alpha metabolism
Cytokines pharmacology
Inflammation chemically induced
Interleukin-1 pharmacology
Tumor Necrosis Factor-alpha pharmacology
Subjects
Details
- Language :
- French
- ISSN :
- 0369-8114
- Volume :
- 41
- Issue :
- 8 Pt 2
- Database :
- MEDLINE
- Journal :
- Pathologie-biologie
- Publication Type :
- Academic Journal
- Accession number :
- 7508593