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Chemical Mediators of Inflammation

Chemical Mediators of Inflammation

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Chemical Mediators of Inflammation

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  1. Chemical Mediators of Inflammation Dr. Raid Jastania

  2. Chemical Mediators of Inflammation • Mediators can be plasma proteins, typically synthesized in the liver and released to the circulation in an inactive form. complement system, Kinins, and coagulation factors. • Mediators can be produced by cells (WBC, endothelial cells, fibroblast). This include arachidonic acid metabolites, cytokines and vasoactive amines.

  3. Chemical Mediators of Inflammation • List of chemical mediators: • Vasoactive amines (eg. histamine) • Plasma proteases (Kinins, Clotting factors, Complement system) • Arachidonic Acid metabolites (PG, Leukotrienes) • Cytokines (Interleukins, chemokines)

  4. Chemical Mediators of Inflammation • act on specific receptor on cell surface. • may induce the production other mediators. • may act by autocrine, paracrine, or endocrine fashion. • may act on one cell type or many cell types. • tightly regulated by their short half-life and by inhibitors. • Mediators may have harmful effect

  5. Chemical Mediators of Inflammation • Histamine: • Source: mast cells • Action: vasodilation and increase vascular permeability by endothelial contraction. • Stimuli: trauma, heat, IgE reaction, C3a, C5a (anaphylatoxins), IL-1, IL-8

  6. Chemical Mediators of Inflammation • Arachidonic Acid metabolites: • Source: phospholipid of cells by the action of Phospholipase A2. • Stimuli: physical, chemical injury, C5a • 2 pathways: • 1.Cyclooxygenase: produce prostaglandins PG, action: vascular changes, pain, platelet function • 2.Lipoxygenase: produce Leukotrienes, eg. LTB4 act as chemotactic agent

  7. Chemical Mediators of Inflammation • Arachidonic Acid metabolites: • Aspirin and NSAID’s inhibit cyclooxygenase activity and result in decrease in PG production and control of pain and fever. • Steroids inhibit Phospholipase A2, and hence all arachidonic acid metabolites.

  8. Chemical Mediators of Inflammation • Cytokines: IL-1, and TNF: • Source: macrophages • Stimuli: injury, immune complex, other mediators • Action: activation of endothelial cells, neutrophils and fibroblasts, They have systemic effect as well.

  9. Chemical Mediators of Inflammation • Cytokines: IL-1, and TNF: • IL-1 and TNF act on the thermoregulatory center in the hypothalamus and induce the production of PGE and result in Fever. • They also enhance the release of WBC’s from the bone marrow and result in Leukocytosis (15,000-20,000 per microliter). • They also induce the bone marrow to produce WBC’s. • IL-6 acts on the liver to increase the production of complement components and coagulation factors.

  10. Morphologic Patterns of Inflammation • Serous Inflammation • Fibrinous Inflammation • Suppurative Inflammation • Ulceration

  11. Morphologic Patterns of Inflammation • Serous Inflammation: • abundant watery effusion fluid (exude/transudate). • Serous inflammation commonly occurs in the serosal surfaces (peritoneum, pericardium, pleura). • Examples: peritonitis, pericarditis, pleuritis, skin burn, viral infections.

  12. Morphologic Patterns of Inflammation • Fibrinous Inflammation: • severe injury to the vessels. • Example: trauma, bacterial infections. • excessive blood clotting and fibrin • organization, • may lead to fibrous adhesions. Example: restrictive pericarditis, fibrous adhesion in the peritoneum.

  13. Morphologic Patterns of Inflammation • Suppurative Inflammation: • pus accumulation (neutrophils, exudate fluid and cellular debris) • typical in bacterial infections eg. staph infection of skin • may lead to abscess formation.

  14. Morphologic Patterns of Inflammation • Ulceration: • Ulcer can be acute or chronic. • Ulceration is necrosis of the epithelial surface (of skin, GIT, respiratory, urogenital tract) with underlying inflammation (acute or chronic). • Peptic ulcer is a typical example. • Ulcer may result from physical or chemical injury, or ischemic necrosis.

  15. Defect in Leukocyte Function • Defect in adhesion: • Leukocyte adhesion deficiency-1 (LAD-1) is a defect in the integrin LFA-1 • Leukocyte adhesion deficiency-2 (LAD-2) is due to absence of sialyl-Lewis X. • Defect in microbial killing: • Chronic granulomatous disease results from defect in oxidative burst function. • Defect in phagolysosome formation • Chediak-Higashi syndrome result from impaired lysosomal degranulation.

  16. Home work • Exercise • Case discussion