INFLAMMATION LECTURE DR HEYAM AWAD, FRCPATH.

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Presentation transcript:

INFLAMMATION LECTURE DR HEYAM AWAD, FRCPATH

INFLAMMATORY REACTION RECOGNITION. RECRUITMENT. REMOVAL OF THE AGENT. REGULATION. RESOLUTION/ REPAIR.

RECOGNITION

RECEPTORS

CELULAR RECEPTORS FOR MICROBES TOLL-LIKE RECEPTORS (TLRs).

WHICH CELLS? EPITHELIAL. DENDRITIC CELLS. MACROPHAGES. WBCs.

SENSORS OF CELL DAMAGE.

SENSORS OF CELL DAMAGE

SENSORS OF CELL DAMAGE

SENSORS OF CELL DAMAGE

SENSORS OF CELL DAMAGE ACTIVATE A PROTEIN CYTOSOLIC COMPLEX CALLES INFLAMMASOME. INFLAMMASOME INDUCES PRODUCTION OF IL-1. IL-1 RECRUITS LEUKOCYTES.

WHICH CELLS? WHERE IN THE CELLS?

OTHER CELLULAR RECEPTORS WBCs EXPRESS RECEPTORS FOR Fc TAIL OF ANTIBODIES AND COMPLEMENT...............SO THEY RECOGNISE MICROBES COATED WITH ANTIBODIES AND COMPLEMENT

CIRCULATING PROTEINS COMPLEMENT SYSTEM REACTS AGAINST MICROBES. MANNOSE- BINDING LECTIN RECOGNISES MICROBIAL SUGARS. COLLECTINS BIND MICROBES.

RECRUITMENT

MARGINATION NORMALLY RBCs ARE CONFINED TO A CENTRAL COLUMN DISPLACING WBCs TO THE PERIPHERY. STASIS CAUSES DECREASE WALL SHEAR STRESS SO MORE WBCs TAKE A PERIPHERAL POSITION.

ROLLING

ROLLING IS FOLLOWED BY ADHESION.

ROLLING AND ADHESION ARE CAUSED BY COMLEMENTARY ADHESION MOLECULES IN BOTH WBC AND ENDOTHELIAL CELLS. ADHESION MOLECULES: SELECTINS AND INTEGRINS.....A LONG STORY!!!

SELECTINS CAUSE ROLLING....WEAK ADHESION. ROLLING SLAWS DOWN WBCs....CHANCE FOR FIRM ADHESION. FIRM ADHESION BY INTEGRING...VCAM AND ICAM

MIGRATION TRANSMIGRATION OR DIAPEDESIS. OCCURS MAINLY IN POSTCAPILLARY VENULES. ADHESION MOLECULES...PECAM (PLATELET ENDOTHELIAL CELL ASHESION MOLECULE). THROUGH THE BASEMENT MEMBRANE? COLLAGENASE.

CHEMOTAXIS CHEMOATTRACTANTS: BACTERIAL PRODUCTS; PEPTIDES AND LIPIDS. CYTOKINES, ESPECIALLY CHEMOKINES( IL8 ). COMPLEMENT C5a. ARACHIDONIC ACID METABOLITES, LEUKOTRIENE B4.

REMOVAL OF INSULT PHAGOCYTOSIS AND INTRACELLULAR KILLING. THREE STEPS : RECOGNITION AND ATTACHMENT, ENGULFMENT, KILLING OR DERGRADATION.

RECEPTORS FOR RECOGNITION MANNOSE RECEPTORS. RECOGNISE MANNOSE AND FUCOSE ON GLYCOPROTEINS AND GLYCOLIPIDS .

RECEPTORS SCAVENGER RECEPTOR. RECOGNISE MODIFIED LDL....OXIDISED OR ACETYLATED.

RECEPTORS RECEPTORS FOR OPSONINS. OPSONINS ARE PROTEINS THAT BIND MICROBES. OPSONINS: IgG, C3b, LECTINS.

ENGULFMENT

INTRACELLULAR DESTRUCTION LYSOSOMAL ENZYMES. REACTIVE OXYGEN SPECIES. REACTIVE NITROGEN SPECIES.

LYSOSOMAL ENZYMES WHICH CELLS?

NEUTROPHIL GRANULES 1. PRIMARY, LARGE, AZUROPHIL GRANULES. MYLOPEROXIDASE, BACTERIOCIDAL FACTORS, HYDROLASES. 2. SECONDARY, SMALL, SPECIFIC GRANULES. LYSOZYME, COLLAGENASE, GELATINASE, ALKALINE PHOSPHATASE, HISTAMINASE.

PROTEASES. ACID PROTEASES....DEGRADE ACIDIFIED DEBRIS . NEUTRAL PROTEASES... CAN DEGRADE COLLAGEN, ELASTIN, FIBRIN, CARTILAGE, BASEMENT MEMBRANE NEUTRAL PROTEASES CAN CAUSE TISSUE DESTRUCTION.

MACROPHAGES CONTAIN: HYDROLASES, COLLAGENASE, ELASTASE, PHOSPHOLIPASE.

ANTIPROTEASES LYSOSOMAL PROTEASES ARE HARMFUL TO OUR TISSUE. CONTROLLED BY ANTIPROTEASES. ALPHA 1 ANTITRYPSIN INHIBITS NEUTROPHIL ELASTASE.

REACTIVE OXYGEN SPECIES OXIDASES CAN PRODUCE ROS, e.g: SUPEROXIDE ANION. OXIDASE CONSISTS OF 7 PROTEINS!! COMPONENTS IN PLASMA MEMBRANE AND CYTOPLASM. ROS PRODUCED IN PHAGOLYSOSOMES.

SUPEROXIDE IS CONVERTED TO HYDROGEN PEROXIDE (H2O2) H2O2 CONVERTED BY MYELOPEROXIDASE TO HYPOCHLORITE (OCL2-) HYPOCHLORITE DESTROYS MICROBES BY HALOGENATION OR OXIDATION.

NITROGEN RADICALS NITRIC OXIDE (NO) PRODUCED BY NITRIC OXIDE SYNTHASE (NOS) NOS...eNOS, nNOS,iNOS. NO RECTS WITH SUPEROXIDE TO FORM PEROXINITRITE(ONOO-)