inate immune system

• Infection


  • Bacteria (E.coli; 7 μm long and 1.8 μm diameter)
  • Virus (20-300 nm)
  • Parasites (Ascaris; 15 to 35 cm, Tapeworm; 30 m)
• A bacterial population can double every 20 minutes – the race is on for the immune system to prevent infection
• Immune System


  • Innate immunity
  • Adaptive immunity
• Innate immunity


  Natural immune response, prevents or limits infection, non-specific
• Adaptive immunity


  Acquired response, eradicates infection, highly specific
• Innate Immune System


  • Physical, chemical and cellular barriers to all infection
• External defences - The skin

  • Layers of closely packed keratinocytes
  • Antimicrobial fatty acids in sebum from sebaceous glands
  • Extracellular antimicrobial lipids; ceramide & sphingosine
  • Acid pH of sweat (lactic acid)
  • Antimicrobial peptides eg dermicidin in sweat from eccrine glands
• Epithelial tight junctions


  • Prevent infection
• Mucus


  • Produced by goblet cells in the epithelium and by mucus glands in the lower respiratory tract
  • Cilia in the lower respiratory tract move the mucus up toward the larynx
  • Epithelial cells produce antimicrobial peptides (defensins) and lysozyme
• Symbiotic bacteria in gut

  • Compete with pathogens for nutrients and sites of attachment
• Other external innate immune defences


  • Flow of tears, urine, saliva, perspiration, vaginal secretions, to prevent microbe adhesion to epithelial surfaces
  • Lysozyme (muramidase) in tears, saliva and mucus
  • Defecation (diarrhea) and vomiting to expel microbes
  • Highly acidic gastric acid secretions (pH 1.2-3.0) destroy bacteria and toxins
• Internal innate immune defences

  • Antimicrobial substances
  • Cellular defences
• Antimicrobial substances


  • Interferons (IFNα, IFNβ, IFNγ), antiviral proteins that inhibit replication of viruses in cells nearby, and limit the spread of the virus
  • Complement proteins, when activated promote bacterial cytolysis, phagocytosis and inflammation
  • Iron binding proteins, eg transferrin and lactoferrin, inhibit the growth of iron-dependent bacteria
  • Antimicrobial peptides (AMPs) such as dermicidin in sweat, defensins produced by epithelial cells, neutrophils and macrophages
• Cellular defences


  • Natural killer (NK) cells; kill virally infected cells which have abnormal proteins in the plasma membrane, by releasing perforin (cytolysis) and granzymes (induce apoptosis). Released microbes are killed by phagocytes.
  • Phagocytes; the neutrophils and macrophages are cells specialised to ingest and destroy microbes.
• Phagocytosis (neutrophils and macrophages)

  1. Phagosome

  2. Phagolysosome
• Symptoms of inflammation


  • Rubor
  • Calor
  • Tumor
  • Dolor
• Stages of inflammation


  1. Vasodilation

  2. Increased vascular permeability

  3. Phagocyte emigration

  4. Tissue repair
• Phagocytes


  • Monocyte
  • Neutrophil
  • Macrophage
• Pus is a pocket of dead phagocytes and damaged tissue that occurs at most sites of inflammation and persists until the bacteria is cleared. Pus can drain externally or internally, for example in patients with massive lung infection.
• Pus


  • Acne
  • Conjuctivitis
• Mediators of vasodilation and increased vascular permeability

  • Histamine released from mast cells activated by complement proteins (C3a and C5a)
  • Bradykinin
  • Prostaglandins
  • Leukotrienes (LTC4)
• Vasodilation and increased permeability causes oedema, but delivers antibodies and coagulation factors from the blood into tissues to limit the spread of infection and improve tissue repair. They also affect nerve endings and cause pain.
• Complement activation in phagocytosis, inflammation and bacterial cytolysis (opsonisation)