AJ

Chapter 16: Innate Immunity: Non-Specific Defenses of The Host

Chapter 16: Innate Immunity: Non-Specific Defenses of The Host

Concept of Immunity

  • Immune System: Protects the human host from pathogens.

  • Immunity: Ability to fight off pathogens and prevent disease.

  • Host Resistance: Presence of immunity; capability of a host to fend off pathogens.

  • Host Susceptibility: Lack of immunity; a state where the host is vulnerable to infection.

  • Host Defense: The entire range of abilities to remove pathogens and prevent disease.

    • Successful host defenses equate to immunity (resistance).

    • Failed defenses lead to disease (susceptibility).

Types of Defenses (Immunity)

Innate Immunity

  • Present at birth; a broad, non-specific defense against all pathogens.

  • Essential for the survival of newborns.

    • Characteristics:

      • Non-specific immunity: Does not discriminate among pathogens.

      • No specific recognition involved: Responds to all pathogens (bacteria, viruses, fungi).

      • Lacks immunological memory: Due to likely first exposure to pathogens.

      • Rapid immune response.

    • Composition:

      • 1st and 2nd Lines of Host Defenses.

Adaptive Immunity

  • Develops later in life; specific to particular pathogens.

    • Characteristics:

      • Specific immunity: Discriminates among pathogens and responds specifically.

      • Has immunological memory: Faster response upon re-exposure to the same pathogen.

    • Composition:

      • 3rd Line of Host Defenses.

Overview of Host Defenses

  • Infection Pathway:

    • Pathogen → 1st Line → 2nd Line of Defense → 3rd Line of Defense.

    • Example:

      • Pathogen → skin/mucous membranes → inflammation/fever → humoral/cellular immunity.

  • Must breach all 3 lines of defense to establish disease.

1st Line of Host Defense: Physical Barriers

  1. Intact Skin:

    • Non-broken, closely packed epithelial cells (flat/tight squamous cells).

    • Continuous layering: Multiple layers in the epidermis.

    • Presence of keratin protein: Reinforces skin integrity to protect underlying layers.

    • Dryness: Less moisture limits pathogen growth.

    • Shedding of the top skin layer: Removes potential pathogens.

  2. Mucous Membranes:

    • Lines body cavities such as gastrointestinal, respiratory, and genitourinary tracts.

    • Secretes viscous fluid (mucus) that traps pathogens.

  3. Ciliary Escalators:

    • Present in the lower respiratory tract; cilia move mucus upward and out of the body.

    • Acts as a flushing mechanism.

      • Mechanism includes actions like coughing or swallowing to remove trapped pathogens.

  4. Lacrimal Apparatus:

    • Protects eyes through tears.

      • Tears continuously wash eyes and remove pathogens.

  5. Saliva, Urine, and Vaginal Secretions:

    • Flushing mechanisms that prevent accumulation of pathogens and wash away potential invaders.

1st Line of Host Defense: Chemical Barriers

  1. Chemical Factors on Skin:

    • pH of Skin: Slightly acidic environment inhibits bacterial growth.

    • Salinity: Hypertonic environment created by salt can cause bacteria to dehydrate and die.

  2. Lysozymes:

    • Enzymes found in secretions (e.g., tears, saliva) that break chemical bonds in peptidoglycan and destroy bacterial cell walls.

    • Effectively kills bacteria lacking peptidoglycan.

  3. Gastric Juices:

    • Produced by the stomach, containing enzymes and acid that destroy most bacteria, except for acidophiles (e.g., D. Archea).

  4. Transferrin:

    • Proteins that bind to iron (Fe) and remove it from circulation, limiting bacterial growth since they require iron to thrive.

1st Line of Host Defense: Biological Barriers

  1. Normal Microbiota:

    • Non-pathogenic microbes that coexist without harming the host.

      • Commensal Microbes: Benefit themselves while the host may not benefit (e.g., certain skin bacteria).

      • Beneficial Microbes: Both host and microbes benefit (e.g., E. coli producing Vitamin K).

      • Opportunistic Microbes: Normal microbiota that can act as pathogens under certain circumstances (e.g., E. coli in the urethra).

      • Competitive Exclusions: Normal microbiota compete with invading pathogens, limiting their population growth by occupying space and utilizing available nutrients, while also producing harmful substances.

2nd Line of Host Defense

  1. Formed Elements in the Blood:

    • Consists of cells and fragments suspended in plasma:

      • Erythrocytes (RBC): Contain hemoglobin to bind oxygen.

      • Leukocytes (WBC): Involved in immune function.

      • Thrombocytes (fragments): Involved in blood clotting, originate from megakaryocytes.

    • Created via hematopoiesis in red bone marrow.

      • Leukocyte Types:

        • Granulocytes (BEN): Have visible granules.

          • Basophils: Release histamine; involved in allergic responses, causing allergy symptoms.

          • Eosinophils: Effective against parasites and helminths.

          • Neutrophils: Phagocytic; first responders to infections, engaging in early-stage defense.

        • Agranulocytes: Lacks visible granules.

          • Monocytes: Travel in blood and mature to macrophages in tissues for phagocytosis.

          • Lymphocytes: Includes T cells, B cells (adaptive immunity), and NK cells.

  2. Phagocytosis:

    • Phagocytosis Definition: The ingestion of microbes or substances by phagocytes.

      • Phagocytes: Non-specific host cells involved in innate immunity (e.g., neutrophils, macrophages).

    • Phagocytosis Mechanism:

      1. Chemotaxis: Chemical signals released by pathogens attract phagocytes.

      2. Adherence: Binding of phagocytes to pathogens.

      3. Ingestion: Endocytosis forms a phagosome, which merges with lysosomes to create a phagolysosome for digestion.

      4. Digestion: Pathogen breakdown occurs within phagolysosomes.

    • Microbial Evasion of Phagocytosis:

      • Pathogens may evade phagocytosis through mechanisms such as capsules, leukocidins (toxins that kill phagocytes), or mycolic acid that inhibits lysosomal enzymes (e.g., Mycobacterium tuberculosis).

  3. Inflammation:

    • Purpose: Attack and remove pathogens, aiding tissue healing with help from neutrophils and macrophages.

    • Causes: Viral/bacterial infection or tissue injury.

    • Signs and Symptoms:

      • Pain: Caused by cytokines damaging nerve endings.

      • Redness (Erythema): Increased blood flow to area.

      • Immobility: Local loss of function due to damaged tissue.

      • Swelling (Edema): Fluid accumulation outside blood vessels due to inflammation.

      • Heat: Increased blood flow to affected area.

    • Inflammation Process:

      1. Tissue damage occurs due to pathogens.

      2. Damaged cells release cytokines.

      3. Cytokines promote phagocyte chemotaxis.

      4. Phagocytes migrate to injury site through blood vessels.

      5. Phagocytosis begins.

      6. Tissue repair initiated.

  4. Fever:

    • Caused by bacterial toxins leading to cytokine release.

    • Cytokines interact with hypothalamus, raising the body temperature set point:

      • Increased set point causes a person to feel chills.

    • Fever leads to abnormally high body temperature until pathogens are eliminated.

    • As cytokines and toxins are cleared, the body temperature may decline—in this phase, called the "crisis" phase, temperature returns to normal.

  5. Antimicrobial Substances:
    (Content from page 8 is not yet provided but expected to elaborate on various antimicrobial agents and substances involved in innate immunity.)