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Inflammation
1. The cellular events of inflammation involve the adhesion of leukocytes to endothelial cells, their migration through blood vessels into tissues, and chemotaxis towards inflammatory stimuli. 2. Phagocytosis is the process by which phagocytes engulf pathogens or debris through opsonization, engulfment, degranulation, and degradation. Phagocytes release reactive oxygen species and enzymes to kill pathogens intracellularly. 3. The resolution of acute inflammation involves demolition of exudates by macrophages, with complete healing and return to normal tissue, or formation of granulation tissue and fibrosis if resolution is delayed. Prolonged inflammation can result in suppuration and abscess formation.
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Inflammation
- 1. INFLAMMATION II CellularEvents
- 2. The cellular exudateFirst exudation of fluid, later leukocytes Exudation of leukocytes A. Adhesion B. Emigration C. Chemotaxis Phagocytosis
- 3. A. Adhesion Normalaxial flow – leukocytes + RBCs, cell free plasma Slowing or stasis -> widening of central stream of cells, narrowing of plasma zone (loss by exudation) White cells impinge upon the endothelium which is sticky and line the endothelial surface (margination of WBCs/pavementation of the endothelium)
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- 5. Adhesion( contd) Leukocyteadhesion molecules – glycoproteins LFA – 1,MO – 1,&p150,95 on the surface of cells Chemical mediator C5a & Leukotreine B4 (LTB4) Endothelial cell receptors stimulated by mediators – endotoxin & interleukin 1 (IL-1), endothelial leukocyte adhesion molecule – 1 (ELAM-1) Intracellular adhesion molecule (ICAM-1) serves as receptor for LFA-1 adhesion molecule on poly, mono, & lymphocytes
- 6. B. Emigration Adherentleukocytes > pseudopodia ↓ between 2 endothelial cells ↓ Basement memb.& perivascular sheath (damaged by collagenases & proteases on surface of migrating cells) First cells involved PMN – 1st 24 hrs -> Monocytes/macrophages – next 24 hrs followed by lymphocytes & RBCs – follow by diapedesis.
- 7. C. Chemotaxis Thedirectional movement of an organism in response to a chemical gradient is chemotaxis Boyden`s chamber experiment
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- 9. Chemotactic facors forleukocytes Leukotriene B4 (LTB4) Platelet activating factor (PAF) Components of complement system – C5a Cytokines( IL8 ) Soluble bact. products (formylated peptides) Monocyte chemoattractant protein (MCP-1) Chemotactic factor for CD4 & Tcells Eosinophil chemotactic factor of anaphylaxis (ECF – A)
- 10. Chemotactic factors Induceleukocyte activation also ↓ - Production of arachidonic acid metabolites -degranulation-> lysosomal enzymes -generation of O2 metabolites - ↑ intracellular Ca -↑ in leukocyte surface adhesion molecules
- 11. Phagocytosis Process ofengulfment of solid particulate material by the cells. Cells ( phagocytes) – 1.PMNs (early ac. Inflammation) 2.Circulating monocytes and fixed tissue mononuclear phagocytes - macrophages
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- 13. Phagocytosis (contd.) Energyfor phagocytosis from anaerobic glycolysis Phagocytosis -> series of metabolic events (Respiratory burst) - ↑utilisation of glucose through hexose monophosphate shunt -> result release of powerful oxidising agents – superoxide radical O2&H2O2 -> intracellular destruction of bacteria Surface phagocytosis – fibrin network >trapping of org. by PNMs without prior opsonisation
- 14. Phagocytosis 4 stepsAttachment stage ( opsonisation) Engulfment stage Secretion ( degranulation stage) Killing or degradation stage
- 15. Attachment stage Phagocytes& micro- org > -vely charged particles > repel each other Opsonins (naturally occuring substances in serum) - IgG opsonin + receptor on the surface of phagocyte (Fc fragment) - C3b opsonin + corresponding receptor on the phagocyte
- 16. Engulfment stage Pseudopodsaround the particle ->Phagocytic vacuole->breaks from cell surface& lies free in cell cytoplasm. PV+lysosomes fuse ->Phagolysosome/ Phagosome.
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- 18. SECRETION(DEGRANULATION STAGE) Preformed granule ->discharged into phagosome Specific granules fuse first- liberate Lysozyme,lactoferrin&alk.PO4ase. Later azurophilic granules fuse->release lysosomal enzymes &PNM ->degranulated
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- 20. SECRETION.contd Mononuclears synthesise& secrete enzymes( interleukins 2&6,TNF->(act as pyrogens->fever)) -arachidonic acid metabolites (prostaglandins,leukotrienes, PAF)& O2metabolites(superoxideO2,H2O2, hypochlorous acid.)
- 21. KILLING or DEGRADATIONSTAGE MICRO-ORGANISMS KILLED BY ANTIBACTERIAL SUBS ARE DEGRADED BY HYDROLYTIC ENZYMES ANTIBACTERIAL AGENTS ACT BY- 1. O2 dependent bactericidal mech.(by prodn. Of reactive O2 metabolites ->(eliminate micro-org. growing within phagocytes )) 2.O2 independent bactericidal mech.- (lysosomal hydrolases, permeability increasing factors,defensins,cationic proteins) 3.Nitric acid mech. In exptal animals- fungicidal & antiparasitic action.
- 22. Activities of PMNin Ac. Infln. RANDOM MOVT. CHEMOTAXIS ADHERENCE TO BACTERIA & PARTICLES PHAGOCYTOSIS ACTIVATION OF HEXOSE MONOPHOSPHATE SHUNT BACTERICIDAL ACTIVITY DEFECT IN ANY OF THESE MECH. ->↓RESISTANCE TO INFN.
- 23. Local sequelae ofac. Infln. Changes following ac. Infln. Depends on : 1. the amount of tissue damage 2. whether or not the causative agent remains. Some agents -> destruction of fixed tissues. If pt. survives,1.autolysis of the area> macrophages infiltrate-> healing by repair & regeneration 2.digestion of the area by lysosomal enzymes of PMN (pus cells) -> abscess. If no tissue death,- PMN -> mononuclears -> onset of demolition phase
- 24. Demolition phase Macrophages (scavengers) engulf-fibrin,red cells ,pus cells, foreign materials, bacteria. - fuse to produce giant cells - act best when activated ( MAF identical to Interferon gamma)↓ bacterial endotoxins phagocytose bacteria
- 25. Functions of macrophagesAntimicrobial defence Immunological functions Cellular immunity Antitumor activity Control of granulopoiesis Control of erythropoiesis Secrtory activity ->lysosomal enzymes, lysozyme,plasminogen activators & inhibitors,collagenases, elastase, complement components,prostaglandins,leukotriens
- 26. End results Resolution– complete return to normal Demolition phase -> removal of exudate – resolution Removal of exudate delayed – fibrin invaded by granulation tissue (organisation) – heals by fibrosis
- 27. End results(Contd.) 2.Suppuration Infl. reaction associated with necrosis -> suppuration Necrotic material > softening > fluid pus in a cavity > abscess Pus – dead & dying leukocytes -- other components of infl. (oedema fluid,fibrin) --organisms (many living – culture) -- tissue debris (nucleic acids & lipids) Epithelial surface involved > ulcer-- floor ->necrotic tissue,ac. Infl. exudate(slough)↓ gets detached– heals by repair ®eneration. Abscess > drained /not drained ↓ dense fibrous tissue,watery content absorbed,calcification.
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