Lecture 17

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Lecture 17
2010-11-11 22:29:26

Host Response to Infection
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  1. Resistance

    • ability to combat disease through body defenses.
    • Resistance is not the same as immunity.

  2. Susceptibility
  3. vulnerability to disease due to a lack or failure of resistance

  • 3 levels of defense against pathogenic microbes.
  • 1. Physical barriers
  • 2. natural, non-specific mechanisms
  • 3. the immune response
  • 1. Physical barriers
    : Epidermis

    • (a layer of epithelial cells) and dermis (underlying connective tissue).
    • Epidermis secretes sebum. Fatty acids and lysozyme are also are present.
  • Physical Barrier: Mucous membranes

    • also consist of epithelial cells (which secrete mucus) and connective tissue.
    • Respiratory mucosa is ciliated and mechanically removes particulates.
  • 2.
    Natural, non-specific mechanisms
    consists of a fluid component (plasma) and formed elements (blood cells & platelets).
  • Blood cells
    Pluripotent stem cells in the bone marrow give rise to all lineages
  • Erythrocytes
    • red blood cells (RBC). Transports bloodgasses & components
  • Leukocytes
    • white blood cells (defense against infection. Five separate lineages)
  • Granulocytes
    Lobular nucleus and numerous cytoplasmic granules.
  • Neutrophils
    Polymorphonuclear cell (PMN, Poly). Most numerous WBC. Phagocytic.
  • Basophil
    Secrete soluble mediators of inflammation and allergic reactions.
  • Eosinophil
    Phagocytic. Active against parasites, but kill worms by release of granule proteins.
  • Monocytes
    Mature, leave blood, enter tissues (macrophages). Largest WBC. Phagocytic.
  • Lymphocytes
    T and B cells are the mediators of the immune response
  • Natural killer cells (NK)
    Active against virally infected cells. IFN augments activity.
  • Platelets
    • clotting factors. Express soluble mediators of inflammation. Megakarocyte
  • Phagocytosis
    Endocytotic ingestion of cells, cell fragments and other insoluble materials.
  • Chemotaxis
    attraction to areas of inflammation and infection.
  • Adherence
    attachment to microbes.
  • Opsonization
    • coating of pathogens with antibodies or complement proteins aids adherence(make easier for cells to eat)
  • Ingestion
    intake to a phagosome or phagocytic vesicle.
  • Fusion
    with a lysosome, to form a phagolysosome.
  • Digestion
    by antimicrobial enzymes (or killing by the respiratory burst (high energy, toxic forms of O2).
  • Inflammation
    A non-specific response to physical, chemical, or infectious agents.
  • Function of inflammation is to
    • 1. Destroy and or remove the injurious agent

    • 2. Confine and limit spread of the agent

    • 3. Repair damaged tissue

  • 5 characteristic manifestations of inflammation
    Redness, heat, swelling, pain, and loss of function
  • 3 stages of inflammation
    1. Vasodilation and increased vascular permeability.
    • The exudate causes edema(water leaves tissues) and pain. Histamines, Prostaglandins, and leukotrienes. -vasodilative amines stimulate these phenomenon.

  • 3 stages of inflammation
    2. Phagocyte migration and activation.
    • Margination-phagocytes stick to endothelium (cells lining vessels)

    • Diapedesis-extravasation to tissues by squeezing between endothelial cells

  • 3 stages of inflammation
    3. Tissue repair
    A process that cannot be completed until all harmful substances are removed. Clinically, there are many types of inflammation, but they reduce to three groups
  • Acute inflammation(tissue repair)
    short duration (days); clears without scarring.
  • Chronic
    longer duration (months to years). Elements of acute reaction are seen with repair, and a scar is seen at the site of the lesion.
  • Granulomatous inflammation
    varying duration, involves the immune system and results in scarring with calcium deposition
  • Fever
    Increased body temperature may inhibit microbes and enhance defense mechanisms.
  • Anti-microbial proteins
    Naturally present or released by cells in response to infection.
  • Transferrin
    an iron-binding protein. Low iron inhibits bacterial growth.
  • Interferons alpha and beta (IFN-alpha and IFN-beta)
    Protects neighbors of virally infected cells.
  • Complement (C')
    A family of more than 20 proteins that act together to express multiple activities. An enzyme cascade system generates an attack complex that makes holes in plasma membranes. Complement also aids phagocytosis and enhances inflammation.