Ch 16 notes REDUCED - Innate Immunity - STUDENT COPY

Introduction to Immunity

  • Nonspecific defenses of the host against infections are termed innate immunity.

Resistance Against Disease

  • Resistance: Ability of the body to ward off disease.

  • Factors contributing to resistance include:

    • Skin

    • Stomach acid

    • Antimicrobial chemicals.

  • Define pathogenic microbial species' properties and host resistance as vital in disease contraction.

The Concept of Immunity

  • Susceptibility: Lack of resistance and vulnerability to disease.

  • Immunity: Ability to ward off disease.

  • Two types of immunity:

    • Innate Immunity: Nonspecific defenses.

    • Adaptive Immunity: Specific defenses against certain pathogens.

Body Defenses Against Infection

  • Pathogens are disease-causing agents that can lead to infections.

  • Three lines of defense:

    1. First Line: Nonspecific defenses (Intact skin, mucous membranes, normal microbiota).

    2. Second Line: Phagocytes, inflammation, fever, and antimicrobial substances.

    3. Third Line: Specific defenses (adaptive immunity) involving T cells and B cells.

First Line of Defense

  • Intact skin

  • Mucous membranes and secretions

  • Normal microbiota.

Second Line of Defense

  • Phagocytes: Neutrophils, eosinophils, dendritic cells, macrophages.

  • Inflammation and Fever as part of the immune response.

  • Antimicrobial substances that target pathogens.

Third Line of Defense

  • Specialized lymphocytes (T cells and B cells).

  • Antibodies: Proteins that bind specifically to antigens to neutralize or eliminate pathogens.

Microbial Evasion of Phagocytosis

  • Mechanisms used by pathogens to evade phagocytosis include:

    • Inhibit adherence: M protein, capsules (Streptococcus pyogenes, S. pneumoniae).

    • Kill phagocytes: Leukocidins (Staphylococcus aureus).

    • Lyse phagocytes: Membrane attack complex (Listeria monocytogenes).

    • Escape phagosome: (Shigella, Rickettsia).

    • Prevent phagosome-lysosome fusion: (HIV, Mycobacterium tuberculosis).

    • Survive in phagolysosome: (Coxiella burnettii).

Recognition of Pathogens by Immune Cells

  • Toll-like receptors (TLRs) and Pattern-recognition receptors (PRRs):

    • Protein receptors on host defensive cells (neutrophils, macrophages, dendritic cells).

    • Recognize pathogen-associated molecular patterns (PAMPs) found on pathogens, including lipopolysaccharides, flagellin, etc.

Differential White Cell Count

  • Normal percentages of white blood cells:

    • Neutrophils: 60–70%

    • Basophils: 0.5–1%

    • Eosinophils: 2–4%

    • Monocytes: 3–8%

    • Lymphocytes: 20–25%

  • Leukocytosis: Increase in white blood cells.

  • Leukopenia: Decrease in white blood cells.

  • Changes vary with infections.

Inflammation

  1. Characteristics of Inflammation: Redness, swelling, heat, and pain.

  2. Major actions during inflammatory response:

    • Vasodilation increases blood flow and permeability, leading to swelling.

    • White blood cells invade the affected area.

    • Tissue fibers enclose the infected area to prevent pathogen spread.

Chemical Mediators of Inflammation

  • Histamine: Causes vasodilation and increased permeability.

  • Kinins, Prostaglandins, Leukotrienes: Intensify the inflammatory response.

Process of Inflammation**

  1. Tissue Damage: Pathogens enter through damaged epidermis, triggering inflammation.

  2. Vasodilation and increased permeability: Blood clot forms; abscesses may develop.

  3. Chemical release: Histamine, kinins, prostaglandins, etc., act to heal the tissue and fight infection.

Phagocyte Migration and Phagocytosis**

  • Margination: Phagocytes adhere to the endothelium of blood vessels.

  • Diapedesis: Phagocytes squeeze through endothelial cells into the tissue to eliminate pathogens.

Tissue Repair**

  • Involves formation of blood clots and regeneration of epidermis and dermis after inflammation.

Fever**

  • Abnormally high body temperature set by the hypothalamus.

  • Caused by gram-negative endotoxins prompting cytokine release.

  • Involves vasoconstriction, increased metabolism, and shivering to raise body temperature.

  • When infection subsides, the temperature returns to normal through vasodilation and sweating.

The Pyrogenic Response**

  • Macrophages ingest bacteria and release cytokines (IL-1 and TNF-α), which induce fever through prostaglandin production.

Benefits of Fever**

  • Interferes with pathogen growth: Reduces iron in blood, slowing pathogen reproduction.

  • Enhances phagocytic activity of white blood cells at higher body temperatures.