1. Define nonspecific resistance
    innate immunity: defences against ANY pathogen
  2. Outline and describe the role of the components of the nonspecific defenses
    • First line of defense: intact skin, mucous membranes and their secretions, normal microbiota
    • Second line of defense: phagocytes, such as neutrophils, eosinophils, dendritic cells, and macrophages, inflammation, fever, antimicrobial substances
  3. Physical factors of the first line of defence (innate)
    • skin: physical barrier (epidermis, dermis)
    • consists of tightly packed cells with keratin
    • dryness inhibits microbial growth (lack of H2O)
    • shedding removes microbes
    • Mucous membranes:
    • mucous traps many microorganisms (+ nose hairs)
    • ciliary escalator moves trapped microorganisms away from lungs
    • epiglottis physically covers lungs
    • cleansing actions - tears, saliva, bodily fluids (urine, vaginal secretions, mucous, semen)
  4. Chemical factors of the first line of defense (innate)
    • Skin: fungistatic fatty-acid in sebum-protective film
    • Lysozyme: in perspiration, tears, saliva, urine, and tissue fluids
    • Low pH: skin (3-5), gastric juice (1.2-3.0), vaginal secretions (3-5)
    • Transferrins: in blood, bind iron
  5. Describe the role of normal microbiota in nonspecific resistance
    • Microbial antagonism/competition against pathogenic microbes
    • 1. physical barrier
    • 2. compete for space/food
  6. Classify phagocytic cells, describe the functions of neutrophils and macrophages
    • Neutrophils, monocytes, macrophages, dendritic cells
    • Neutrophils: protects against microbes during initial phase of infection
    • Macrophages: develop from monocytes, dominate as infection progresses
  7. Explain the process of phagocytosis
    • Host TLRs attach to PAMPs
    • Chemotaxis and adherance of microbes to phagocyte
    • Ingestion from pseudopods
    • Formation of phagosome
    • Formation of phagolysosome (phagosome + lysosome)
    • Digestion of microbe
    • Residual body contains indigestible material
    • Discharge of waste
  8. Describe the stages of inflammation
    • Response to tissue damage - intended to limit damage and restore function
    • Signs and symptoms include redness, pain, heat, and swelling
    • Tissue damage: release of chemical mediators trigger vasodilation, blood clot forms, absess starts to form,
    • Vasodilation: increased vascular permeability
    • Phagocyte migration and phagocytosis: [first neutrophils then macrophages] margination (phagocytes stick to endothelium), diapedesis, phagocytosis of invading bacteria
    • Tissue repair: scab, blood clot, regenerated epidermis, regenerated dermis
  9. Describe the cause and effects of fever
    • Pyrogens (fever inducing endotoxins) cause phagocytes to release IL-1, which causes the hypothalamus to release prostaglandins which reset the hypothalamus to a higher temperature
    • When fever increases rate of metabolism increases, however sweating causes fever to go down.
    • Advantages: speeds up tissue repair, increase in speed/activation of other body defenses
    • Disadvantages: tachycardia, acidosis, dehydration, too high can be fatal
  10. Discuss the role of complement activation and 3 consequences.
    • Serum proteins are activated in a cascade
    • 1. Opsonization: C3b enhances phagocytosis
    • 2. Inflammation: C3a + C5a
    • 3. Cytolysis: C5b + C6 + C7 + C8 + C9 membrane attack complex
  11. Antimicrobial substances
    • Interferons: inhibit viral replication
    • Transferins: host protein, bind serum iron
    • Antimicrobial peptides: lyse bacterial cells
  12. Interferons
    • Properties: short lived, antiviral, specific to host cell NOT to virus
    • Function: inhibit viral replication in surrounding cells
    • Mechanism: binds to surface of surrounding cells causing them to secrete antiviral proteins
    • Alpha  IFN: leukocytes
    • Beta IFN: fibroblast (connective tissues)
    • Gamma IFN: lymphocytes (enhances ability to phagocitize bacteria)
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