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2. inflammation cellular events dr ashutosh kumar

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2. inflammation cellular events dr ashutosh kumar

  1. 1. summary Inflammation-acute and chronic Acute - cardinal sign stimuli changes -vascular & cellular•vascular- vasodilation; increased vascular permeability transcytosis
  2. 2. ACUTE INFLAMMATION- CELLULAR EVENTS “AIM IS TO DELIVER LEUCOCYTES TO THE SITE OF INJURY” LUMINAL  MARGINATION  ROLLING  ADHESION TRANSMIGRATION ACROSS ENDOTHELIUM MIGRATION IN INTERSTITIAL TISSUES
  3. 3. STEPS OF EXTRAVASATION OF INFLAMMATORY CELLS
  4. 4. ACUTE INFLAMMATION- CELLULAR EVENTS MARGINATION- Increased No. Of WBCs In The Periphery Adjacent To Endothelium ROLLING- Slow Tumbling And Transient Adhesion PAVEMENTING- Complete Lining Of Endothelium By WBCs
  5. 5. LEUCOCYTE ADHESION AND TRANSMIGRATION-MECHASINMS DUE TO ADHESION MOLECULES 4 CLASSES OF ADHESION MOLECULES Selectins Immunoglobulin class Integrins Mucin like glycoproteins
  6. 6. ADHESION MOLECULES SELECTINS ADHESION OF LEUCOCYTES TO ENDOTHELIAL CELLS E-SELECTINS  On endothelial cells  Bind to CHO groups on granulocytes,monocytes.Memory T cells P-SELECTINS  Endo And Platelets  Bind Neutro,T-Lymphos, monos L-SELECTINS  impt in homing
  7. 7. ADHESION MOLECULES IMMUNOGLOBULIN CLASS EXPRESSED ON ENDOTHELIAL CELLS ICAM-1:INTERCELLULAR ADHESION MOLECULE VCAM-1:VASCULAR CELL ADHESION MOLECULE ACT AS LIGANDS TO INTEGRINS
  8. 8. ADHESION MOLECULES INTEGRINS HETERODIMERIC CELL SURFACE PROTEINS + ON MANY CELLS CELL-CELL AND CELL-MATRIX INTERACTIONS
  9. 9. ENDOTHELILI LEUKOCYTE MOLECULE ROLEAL MOLECULEGLYCAM1 L-selectin ROLLINGP- SELECTIN Sialyl-Lewis X–modified proteins ROLLINGE-SELECTIN Sialyl-Lewis X–modified proteins ROLLING+ ADHESIONV CAM 1 CD11/CD18 (β2) integrins (LFA-1, ADHESION Mac-1)I CAM 1 VLA-4 (β1) integrin ADHESION+ TRINSMIGRATIO N
  10. 10. Innflammation induces redistribution ofadhesion molecules
  11. 11.  leukocyte adhesion deficiency type 1: defective biosynthesis of the β2 chain shared by the LFA-1 and Mac-1 integrins. Leukocyte adhesion deficiency type 2: d/t absence of sialyl-Lewis X,
  12. 12. Stages of Phagocytosis: Chemotaxis: DEFINITION- Process Of Directed Cell Migration Along A Chemical Gradient Responsible for emigration of leucocytes towards the site of injury
  13. 13. CHEMOTAXIS-AGENTS EXOGENOUS  BACTERIAL PRODUCTS-COMMONEST  PEPTIDES OR LIPIDS ENDOGENOUS  COMPLEMENT COMPONENTS-C5a  LEUKOTRIENE B4  CYTOKINES-IL-8
  14. 14. CHEMOTAXIS-MECHANISM Bind to specific receptors on leucocytes Effector molecules produced-phospholipase, tyrosinase etc Second messengers-finally leading to polymerization of actin Leucocyte moves by extending filopodia
  15. 15. Neutrophil Crawling on a Glass Slide It is going that way:
  16. 16. RECRUITMENT OF LEUCOCYTES TO SITE OF INJURY INITIAL 6-24 HOURS– NEUTROPHILS LATER-- MONOCYTES
  17. 17. Recognition of Microbes and Dead Tissues
  18. 18. Phagocytes are Attracted to Site of Infection by Chemotaxis
  19. 19. Stages of Phagocytosis: Adherence: Phagocyte plasma membrane attaches to surface of pathogen or foreign material.  Adherence can be inhibited by capsules (S. pneumoniae) or M protein (S. pyogenes).  Opsonization: Coating process with opsonins that facilitates attachment.  Opsonins include antibodies and complement proteins.
  20. 20. Stages of Phagocytosis (Cont…)3. Ingestion: pseudopods formation: lead to engulfment of the microbe4. Digestion: phagolysosome formation. Lysosomal enzymes includes: Lysozyme: Destroys cell wall peptidoglycan Lipases and Proteases RNAses and DNAses After digestion, residual body with undigestable material is discharged.
  21. 21. Process of Phagocytosis
  22. 22. KILLING AND DEGRADATION O2 DEPENDENT-MORE IMPORTANT O2 INDEPENDENT
  23. 23. O2 DEPENDENT MECHANISMS Phagocytosis stimulates burst of oxygen consumption Production of ROS Superoxide produced during oxidation of NADPH Superoxide converted to H2O2 Further reduced to hydroxyl radical
  24. 24. O2 DEPENDENT MECHANISMS Hydrogen peroxide not very effective by itself Converted by MPO in presence of Cl to form HOCl (hypochlorite)
  25. 25. O2 INDEPENDENT MECHANISMS Bacterial permeability increasing protein- phospholipase activation Lysozyme Lactoferrin Major basic protein-for parasites Elastase
  26. 26. DEGRADATIONAfter killing microbes are degraded in lysosomes by acid hydrolases
  27. 27. LEUCOCYTE INDUCED TISSUE INJURY Protector becoming offender Release of microbicidal products into EC space Endothelial injury and tissue necrosis Amplify inflammation Eg.-ARDS, acute transplant rejection, glomerulonephritis
  28. 28. INFLAMMATION: REGULATION
  29. 29. DEFECTS IN LEUCOCYTE FUNCTION GENETIC ADHESION DEFECTS-  LAD1, LAD2  INTEGRINS AND SELECTIN RECEPTORS DEFECTIVE  REC BACTERIAL INFECTIONS AND IMPAIRED HEALING DEFECTS IN PHAGOLYSOSOME FUNCTION  CHEDIAK HIGASHI SYN  AR  DEFECTIVE TRANSFER OF LYSOSOMAL ENZYMES
  30. 30. DEFECTS IN LEUCOCYTE FUNCTION DEFECT IN MICROBICIDAL ACTIVITY  CGD-DEFECTS IN NADPH OXIDASE  REC BACTERIAL INFECTIONS MPO DEF ACQUIRED-VARIOUS ASPECTS LIKE PHAGO,CHEMO ETC AFFECTED DM MALIGNANCY MALNUTRITION ANEMIA

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