Innate immunity

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  • Innate Immunity
    • 1. Physical Barriers
      • Skin
        • Dead cells + bacteria
        • Sebaceous glands
          • fatty acids
          • Lactic acid
          • low pH (3-5) - to inhibit microbial growth
        • Very dry - preventing microbial growth
      • Mucous membrane
    • 2. Physiological Barriers
      • pH and environment
        • low pH in gut to prevent pathogen growth
      • Fever
        • prevent pathogen growth
        • Speegs up phagocytosis
      • Chemical Mediators
        • Complement poteins - lysis of invading bacteria
        • Anti-microbial proteins e.g. lysozyme in tears
        • Interferon - induces anti-viral state in cells (inhibit viral reproduction in cells)
    • 3. Phagocytosis
      • Neutrophils, macrophages, eosinophils
        • Fc receptors - antibody conded receptor
      • Dendritic cells
        • Ganulocytes - myeloid lineage
      • Two mechanisms
        • Oxygen-dependent killing
          • Nitric oxide synthetase is activated
          • Nitric oxide is generated
            • Acts as anti-microbial
        • Oxygen-independent Kiling
          • Lysozyme - hydrolytic enzyme
          • Defensins - peptides kill many bacteria
            • Punch holes in bacterial cell wall
      • Pseudopodia (receptors recognise bacerial cell wall compnent
    • 4. Inflammation
      • Increased blood supply, increased blood vessel permeability, increased leukocyte migration to the area
        • Macrophages and cytokines
      • 1. Chemokine Release
        • IL-8 release from damaged endothelial cells and TNF-alpha release from macrophages help to recruit neutrophils and allow migration from blood
          • Interleukin is a cytokine
        • Histamine release from mast cells causes vasodilation and increase blood vessel permeability
      • 2. Activation of clotting and complement cascade
        • Releases more histamine, attracting more phagocytic cells
      • 3. Neutrophils secrete cytokines to recruit macrophages
      • 5. Macrophages migrate to tissue and secrete IL-1 and TNF-alpha to recruit lymphocytes, monocytes and neutrophils
      • Systemic acute-phase response
        • Fever
        • Leukocytosis ( white cell production increase)
        • Acute phase proteins production by liver
          • Binds to microbes, activates complement proteins which aid PHAGOCYOTSIS
            • Coating - opsonisation
    • Rapid response but full adaptive response can take up to 10 days
    • Highly conserved - present in all animals, plants and fungi
  • E.g. respiratory mucous membrane
    • Mucous membrane
  • Anti-microbial peptides e.g. defensin - damage pathogens - small proteins with +ve charge
    • Chemical Mediators
      • Complement poteins - lysis of invading bacteria
      • Anti-microbial proteins e.g. lysozyme in tears
      • Interferon - induces anti-viral state in cells (inhibit viral reproduction in cells)
  • 4. Phagocytosis of pathogens
    • 4. Inflammation
      • Increased blood supply, increased blood vessel permeability, increased leukocyte migration to the area
        • Macrophages and cytokines
      • 1. Chemokine Release
        • IL-8 release from damaged endothelial cells and TNF-alpha release from macrophages help to recruit neutrophils and allow migration from blood
          • Interleukin is a cytokine
        • Histamine release from mast cells causes vasodilation and increase blood vessel permeability
      • 2. Activation of clotting and complement cascade
        • Releases more histamine, attracting more phagocytic cells
      • 3. Neutrophils secrete cytokines to recruit macrophages
      • 5. Macrophages migrate to tissue and secrete IL-1 and TNF-alpha to recruit lymphocytes, monocytes and neutrophils
      • Systemic acute-phase response
        • Fever
        • Leukocytosis ( white cell production increase)
        • Acute phase proteins production by liver
          • Binds to microbes, activates complement proteins which aid PHAGOCYOTSIS
            • Coating - opsonisation

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