Inflammation PDF
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Uploaded by InnocuousSilver3002
University of Plymouth
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Summary
This document provides a comprehensive overview of inflammation, including various mediators and pathways. It covers aspects like extravasation, cell-derived mediators, pain pathways, and the role of key factors in inflammation.
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INFLAMMATION Extravasation -- recruits immune cells to injury -\> rapid Mast cell = histamine -\> vascular permeability Macrophages = IL-8 -- recruits neutrophils Monocyte becomes macrophage when it leaves the blood vessel Plasma derived mediators: - Clotting system - Kinin system - Fi...
INFLAMMATION Extravasation -- recruits immune cells to injury -\> rapid Mast cell = histamine -\> vascular permeability Macrophages = IL-8 -- recruits neutrophils Monocyte becomes macrophage when it leaves the blood vessel Plasma derived mediators: - Clotting system - Kinin system - Fibrinolytic system (plasmins) - Complement system Cell derived mediators: - Auxiliary cells -\> basophils, mast cells, platelets - Lymphocytes - Monocytes Kinins: - Release NO = venous dilation + vascular permeability - Activated by Hageman factor (XIIa) in clotting cascade, plasma system, enzymes from dmg tissues - Produces bradykinin + lysyl-bradykinin Plasmin: - Converts plasminogen into plasmin - Plasmin activates MMP -\> tissue remodelling - Promote angiogenesis by cytokine release - Breaks down fibrin -\> dissolves clot after bleeding stops Cell-derived mediators: - Mast cells, basophils, platelets - Activated C3a + C5a (innate) and IgE (adaptive) - Rapid release of histamine + serotonin (stored in platelets) (degranulation) - Increased vasodilation + permeability - Slow release of leukotrienes and prostaglandins - \- activated by immune complexes (antibodies) - Platelet activating factor (PAF) -\> neutrophils, basophils, macrophages - Type 1 + 2 hypersensitivity - Recruitment + activation of other immune cells - CCL3 (MIP1-a) + leukotriene B4 (chemotactic for monocytes) - Chemokines \_ cytokines modulate local immune responses Pain: - PAF, histamine, serotonin, prostaglandin, leukotrienes - Act on C fibres - Poorly localised, dull, aching pain Arachidonic acid pathway: - Important factor in generation of key inflam mediators prostaglandid + leukotrienes - Corticosteroids cut out entire pathway = no inflammation - Ibuprofens stop COX pathway, but also reduces bloodflow to stomach = stomach ulcers - Aspirin = blood thinner, restricts cyclooxygenase pathway + TXA2 = vasodilation -\> mainly affects COX2 - Xylotol = 5-lipoxygenase inhibitor - Montelukast = blocks leukotriene receptor - Leukotrienes = airway tightening, vascular permeability, inflammation inhibition
