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Chronic Inflammation PowerPoint Presentation

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Published on : Aug 07, 2014
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Slide 1 - Chronic Inflammation and Mediators
Slide 2 - Summary of acute inflammation Stimulated by physical injury, infection, foreign body Initiated by resident macrophages and/or damaged endothelium IL-1, TNF, endothelin, histamine initiate vascular response—vasodilation, endothelial contraction, exudation of plasma Neutrophils marginate (selectin-glycoprotein), adhere (integrin-CAM), extravasate (CD31), migrate (IL-8, chemotactic stimuli) Phagocytosis: recognition, engulfment, killing Phagocytosis receptors bind mannose, oxidized lipids, lipopolysaccharides, lipoteichoic acids, opsonins Killing is O2-dependent (respiratory burst, NADPH oxidase generated H2O2; myeloperoxidase generated HOCl; iNOS generated NO) or independent (lysozyme, lactoferrin, defensins) Responding leukocytes cause pain and loss-of-function via enzymes, prostaglandins Complete resolution; fibrosis, organization or scarring; abcess formation; progression
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Slide 4 - Margination PMN's that are marginated along the dilated venule wall (arrow) are squeezing through the basement membrane (the process of diapedesis) and spilling out into extravascular space.
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Slide 7 - Acute bronchopneumonia
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Slide 9 - Chronic inflammation Chronic inflammation is prolonged (weeks or months) Inflammation, tissue injury, and attempts at repair coexist, in varying combinations May follow acute inflammation May begin insidiously without any manifestations of an acute reaction
Slide 10 - Causes of chronic inflammation Persistent infections Organisms usually of low toxicity that invoke delayed hypersensitivity reaction M. tuberculosis and T. pallidum causes granulomatous reaction Prolonged exposure to potentially toxic agents Exogenous agents include silica which causes silicosis Endogenous causes include atherosclerosis caused by toxic plasma lipid components Autoimmunity Auto-antigens provoke self-perpetuating immune responses that cause chronic inflammatory diseases like RA, MS Responses against common environmental substances cause chronic allergic diseases, such as bronchial asthma
Slide 11 - Histologic features Infiltration with mononuclear cells (eg. macrophages, lymphocytes and plasma cells) due to persistent reaction to injury Tissue destruction induced by persistent agent or inflammatory cells Attempts at healing by connective tissue replacement of damaged tissue with angiogenesis and fibrosis
Slide 12 - Chronic inflammation
Slide 13 - Acute inflammation
Slide 14 - eosinophils, plasma cells, and macrophages
Slide 15 - Macrophages in chronic inflammation Mononuclear phagocytes arise from a common precursor in the bone marrow From the blood, monocytes migrate into various tissues and differentiate into macrophages The half-life of blood monocytes is about 1 day The life span of tissue macrophages is several months or years Monocytes begin to emigrate into extravascular tissues quite early in acute inflammation In chronic inflammation, macrophage accumulation persists as a result of continuous recruitment from the circulation and local proliferation at the site of inflammation
Slide 16 - Resident and activated macrophages Kupffer cells - liver Sinus Histiocytes - spleen and lymph nodes Alveolar Macrophages – Lungs Microglia – brain
Slide 17 - Lymphocytes in chronic inflammation T and B cells Cytokines from activated macrophages, mainly TNF, IL-1, and chemokines, promote leukocyte recruitment Macrophages display antigens to T cells and produce membrane molecules (costimulators) and cytokines (notably IL-12) that stimulate T-cell responses Activated T lymphocytes recruit monocytes from the circulation with IFN-γ, a powerful activator of macrophages Plasma cells develop from activated B lymphocytes and produce antibodies Accumulations of lymphocytes, antigen-presenting cells, and plasma cells may assume the morphologic features of lymph nodes, called tertiary lymphoid organs
Slide 18 - Other cells in chronic inflammation Eosinophils abundant in immune reactions mediated by IgE and in parasitic infections, recruited by eotaxin granules contain major basic protein, a highly cationic protein that is toxic to parasites but also causes lysis of host epithelial cells Mast cells express on their surface the receptor (FcεRI) that binds the Fc portion of IgE antibody granules release histamine and prostaglandins during allergic reactions to foods, insect venom, or drugs, sometimes with catastrophic results (e.g. anaphylactic shock) Neutrophils induced either by persistent microbes or by mediators produced by activated macrophages and T lymphocytes neutrophilic exudate can persist for many months in osteomyelitis cause chronic damage induced in lungs by smoking and other irritant stimuli
Slide 19 - Granulomatous inflammation Focus of chronic inflammation encountered in a limited number of conditions Cellular attempt to contain an offending agent that is difficult to eradicate (i.e. Tb) Consists of a microscopic aggregation of macrophages that are transformed into epithelioid cells, surrounded by a collar of mononuclear leukocytes, principally lymphocytes and occasionally plasma cells Epithelioid cells have a pale pink granular cytoplasm with indistinct cell boundaries, often appearing to merge into one another as giant cells Foreign body granulomas are incited by relatively inert foreign bodies (i.e. talc, sutures) Immune granulomas are caused by several infectious agents that provoke a cell-mediated immune response
Slide 20 - Causes of granulomas
Slide 21 - Foreign body granuloma
Slide 22 - Granuloma
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Slide 24 - Mediators of inflammation Vasoactive amines Plasma proteases Clotting system Fibrinolytic system Kinin system Complement system Arachidonic acid metabolites Eicosanoids Prostaglandins Leukotrienes Platelet Activating Factor Cytokines ROS and NO Lysosomal constituents Vasodilation Prostaglandins NO Vascular permeability Vasoactive amines C3a and C5a Bradykinin Leukotrienes C4, D4, E4 Chemotaxis C5a Leukotriene B4 Bacterial products Chemokines (IL-8) Fever IL-1, IL-6, TNFa Bradykinin Tissue damage ROS and NO Lysosomal constituents
Slide 25 - Vasoactive amines Histamine causes dilation of arterioles and increases the permeability of venules mediated mainly via binding to H1 receptors on microvascular endothelial cells liberated from blood basophils and connective tissue mast cells in response to Injury, heat and cold binding of specific antigen to membrane-bound IgE binding of complement fragments C3a and C5a anaphylotoxins Interleukin-1, IL-8 Factors from neutrophils, monocytes and platelets Serotonin also known as 5-hydroxytryptamine acts like histamine and derived from platelets
Slide 26 - Prostaglandins, Leukotrienes, Lipoxins Receptor binding, kinase activation, Ca release activates PLA2 Arachidonic Acid (AA) liberated from plasma membrane Cyclo-oxygenase activity (constitutive and inducible COX-1 and COX-2) makes prostaglandins PGI2 and (PGF1α) is a vasodilator, a potent inhibitor of platelet aggregation, and also markedly potentiates the permeability-increasing and chemotactic effects of other mediators TxA2, a potent platelet-aggregating agent and vasoconstrictor, is unstable and rapidly converted to inactive TxB2 PGD2 (mast cells) and PGE2 (more widely distributed) cause vasodilation and increase the permeability of post-capillary venules PGD2 is a chemoattractant for neutrophils PGE2 causes pain Lipoxygenase activity makes leukotrienes and lipoxins LTB4 is a potent chemotactic agent and activator of neutrophils, causing aggregation and adhesion of the cells to venular endothelium, generation of ROS, and release of lysosomal enzymes Cysteinyl-containing leukotrienes C4, D4, and E4 (LTC4, LTD4, LTE4) cause intense vasoconstriction, bronchospasm, and increased vascular permeability in venules Lipoxins are anti-inflammatory
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Slide 28 - Cytokines and Chemokines
Slide 29 - Plasma proteases Clotting cascade XII (Hageman factor) Complement cascade C3a and C5a Kinin system Hageman factor, kallikrein Plasmin and bradykinin
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Slide 32 - Important mediators of inflammation
Slide 33 - Describing inflammation Morphological diagnosis using four-word term Duration Distribution, pattern Character Location, organ
Slide 34 - Duration of the process acute indicates a process that began recently chronic indicates a process with an extended time course any fibrosis (collagen deposition) is chronic because it takes days to occur subacute is an inbetween term, possibly in the vicinity of 3-7 days
Slide 35 - Distribution of the lesion focal means in a single spot or region multifocal means similar lesions are scattered in many spots diffuse indicates that the lesion is distributed evenly throughout most or all of the examined tissue
Slide 36 - Character of the exudate suppurative indicates a prominent component of neutrophils lymphocytic, plasmacytic, and lymphoplasmacytic indicate a lack of neutrophils and a predominence of lymphoid cells granulomatous inflammation is always chronic, and contains large, reactive, epitheloid macrophages
Slide 37 - Location and presence of inflammation Terms combine the organ name as a root with the suffix “itis” tonsillitis, apendicitis, dermatitis, hepatitis, placentitis, nephritis (kidneys), mastitis (mammary glands), orchitis (testis), cholecystitis (gall bladder), etc. a few tissues have atypical terms pneumonia and pleurisy
Slide 38 - Examples of morphologic diagnoses acute diffuse suppurative enteritis inflammation that includes the entire mucosal surface of the small intestine, which began recently and contains neutrophils acute suppurative inflammation suggests a bacterial infection, such as Salmonella or Campylobacter subacute multifocal lympoplasmacytic meningoencephalitis inflammation in multiple scattered spots throughout the brain and meninges, perhaps a week in duration, containing lymphocytes and plasma cells this type of inflammation is suggestive of a viral infection, perhaps West Nile virus, St. Louis Encephalitis virus, or rabies chronic focal granulomatous pneumonia isolated lesion in the lung that is suggestive of tuberculosis