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Immunity to bacteria

Immunity to bacteria. Barrier defenses of human body. Antibacterial Responses. “ Protection is initiated on activation of innate responses on a local basis and progress to acute-phase and antigen specific responses on a systemic scale ”. major events in acute inflamation.

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Immunity to bacteria

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  1. Immunity to bacteria

  2. Barrier defenses of human body

  3. Antibacterial Responses “Protection is initiated on activation of innate responses on a local basis and progress to acute-phase and antigen specific responses on a systemic scale”

  4. major events in acute inflamation • Expansion of capilaries to increase blood flow (seen as blushing or a rash) • Increase in the permeability of the microvasculature structure to allow escape of fluid, plasma proteins, and leukocytes from the circulation edema • Exit of leukocytes from the capillaries and their accumulation at the site of injury

  5. Bacterial components that activate Protective Responses I • Direct activation • LPS • Lipoteichoic acid • Lipoarabinomannan • Glycolipids and glycopeptides • Polyanions • N-Formyl peptides

  6. Bacterial components that activate Protective Responses II • Chemotactic • Peptidoglycan fragments • Cell surface activation of alternative pathways of complement (C3a, C5a)

  7. Complement in antibacterial response • Alternative and Lectin pathways activated by bacterial surfaces • Classic pathway activated later by antibody-antigen complexes • Production of chemotactic and anaphylotoxic proteins (C3a, C5a) • Opsonization of bacteria (C3b) • Promotion of killing of gram-negative bacteria • Activation of B cells (C3d)

  8. Complement cascade

  9. Neutrophil diapedesis in response to inflamatory signals

  10. Phagocytes & Phagocytosis • PMNs, monocytes, and eosinophilsare the first cells to appear in response to acute inflammation; they are followed later by macrophages

  11. Neutrophils • major antibacterial response • an increased number of neutrophils in the blood, body fluids or tissue indicates: “bacterial infection” • “left shift”

  12. Steps in Phagocytosis • Attachment • bacterial carbohydrates (lectins) • receptor for opsonins • fibronectin receptors • Fc receptors • Internalization (phagocytic vacuole) • Digestion (phagosome)

  13. Antibacterial compounds of the phagolysosome I • Oxygen-dependent compounds • Hydrogen peroxide: NADPH oxidase and NADH • Superoxide • Hydroxil radicals (OH) • Activated halides (Cl_, I_, Br_): myeloperoxidase • Nitrous oxide

  14. Antibacterial compounds of the phagolysosome II • Oxygen-independent compounds • Acids • Lysosome (degrades bacterial peptidoglycan) • Lactoferrin (chelates iron) • Defensin and other cationic proteins (damage membranes) • Proteases, elastase, cathepsin G

  15. Phagocytosis & killing of bacteria

  16. Macrophages in antibacterial response • Important antibacterial phagocytic cells • Killing by oxygen-dependent and oxygen-independent mechanisms • Production of IL-1, IL-6, and IL-12; TNF-a and TNF-b, and interferon-a • Activation of acute-phase and inflammatory responses • Presentation of antigen to CD4 T cell

  17. Antibacterial responses

  18. a1-antitrypsin a1-glycoprotein Amyloid A & P Antithrombin III C-reactive protein C1 esterase inhibitor C3 complement Ceruloplasmin Fibrinogen Haptoglobulin Orosomucoid Plasminogen Transferrin Lypopolysaccharide-binding proteins Acute-Phase Reactants

  19. Specific Immune Responses to Bacteria I • Macrophages move to lymph nodes and interact with CD4 T cells after ingestion of bacteria • initially: Macroph(APC). CD4 TH0 cells antigenic peptides + class II MHC TCR + CD4, on TH0

  20. Specific Immune Responses to Bacteria II • costimulatory signals from the interaction of CD28 (T cells) B7 molecule (macrophage) + IL-1, IL-12 • TH0 produce IL-2, IFN-g and IL-4 • B cells produce IgM • LPS and cell wall polysaccharides activate B cells

  21. Specific Immune Responses to Bacteria III • TH0 TH1 (IL-12 & IFN-g) • activation of Macrophages, T cells, B cells • important for intracellular infections • CD4 TH2 T-cell response • occur later • initiated by the B cell presentation of antigen • presentation to TH2 cell (Ag + class II MHC) • TH2 IL-4, IL-5, IL-6, IL-10 IgG , Plasma-cells, memory cells

  22. T cells in antibacterial response • TH1 CD4 responses important for intracellular bacterial infections • TH2 CD4 response important for all bacterial infections • CD8 cytolytic T cells not very important

  23. Antibody in antibacterial response • primary protection against extracellular bacteria and reinfection • Binding to surface structures of bacteria (fimbriae,lipoteichoic acid, capsule) • Blocking attachment • Opsonization of bacteria for phagocytosis • Promotion of complement action • Promotion of clearence of bacteria • Neutralization of toxins and toxic enzymes

  24. Bacterial Immunopathogenesis “tissue and systemic damage” • IL-1, IL-6 and TNF-a life-threatening in systemic infection • endotoxin macrph. TNF-a in the blood symptomes of sepsis • antibodies which share determinants with human proteins post-streptococcal glomerulonephritis and rheumatic fever • superantigens STSS

  25. Bacterial Evasion of Protective Responses • the inhibition of phagocytosis and intracellular killing in the phagocyte • inactivation of complement function • cleavage of IgA • intracellular growth (avoidance of antibody) • change in bacterial antigenic appearence

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