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Nonspecific Defenses of the Host

Nonspecific Defenses of the Host. Susceptibility: Lack of resistance to a disease. Immunity: Ability to ward off disease. Innate immunity: Defenses against any pathogen. Adaptive immunity: Immunity, resistance to a specific pathogen. Host Defenses. Figure 16.1. Physical Factors. Skin

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Nonspecific Defenses of the Host

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  1. Nonspecific Defenses of the Host • Susceptibility: Lack of resistance to a disease. • Immunity: Ability to ward off disease. • Innate immunity: Defenses against any pathogen. • Adaptive immunity: Immunity, resistance to a specific pathogen.

  2. Host Defenses Figure 16.1

  3. Physical Factors • Skin • Epidermis consists of tightly packed cells with keratin, a protective protein

  4. Physical Factors • Mucous membranes • Ciliary escalator: Microbes trapped in mucus are transported away from the lungs. • Lacrimal apparatus: Washes eye. • Saliva: Washes microbes off. • Urine: Flows out. • Vaginal secretions: Flow out. Figure 16.4a

  5. Chemical Factors • Fungistatic fatty acid in sebum. • Low pH (3-5) of skin. • Lysozyme in perspiration, tears, saliva, and tissue fluids—what does it do? • Low pH (1.2-3.0) of gastric juice. • Transferrins in blood find iron. • NO inhibits ATP production.

  6. Normal Microbiota • Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens.

  7. Formed Elements in Blood Table 16.1 (1 of 2)

  8. Formed Elements in Blood Table 16.1 (2 of 2)

  9. Differential White Cell Count • Percentage of each type of white cell in a sample of 100 white blood cells.

  10. White Blood Cells • Neutrophils: Phagocytic • Basophils: Produce histamine • Eosinophils: Toxic to parasites (worms), phagocytosis • Dendritic cells: Initiate adaptive immune response • Monocytes: Phagocytic as mature macrophages • Fixed macrophages in lungs, liver, and bronchi • Wandering macrophages roam tissues. • Lymphocytes: Involved in specific immunity.

  11. Phagocytosis • Phago: from Greek, meaning eat • Cyte: from Greek, meaning cell • Ingestion of microbes or particles by a cell, performed by phagocytes. Figure 16.6

  12. Phagocytosis Figure 16.7

  13. Microbial Evasion of Phagocytosis

  14. Inflammation • FOUR CARDINAL SIGNS: • Redness • Pain • Heat • Swelling (edema) • Acute-phase proteins activated (complement, cytokine, and kinins) • Vasodilation (histamine, kinins, prostaglandins, and leukotrienes) • Margination and emigration of WBCs • Tissue repair

  15. Chemicals Released by Damaged Cells

  16. Inflammation Figure 16.8a–b

  17. Inflammation Figure 16.8c–d

  18. Fever: Abnormally High Body Temperature • Hypothalamus normally set at 37°C. • Gram-negative endotoxin cause phagocytes to release interleukin–1 (IL–1). • Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature. • Body increases rate of metabolism and shivering which raise temperature. • When IL–1 is eliminated, body temperature falls (crisis).

  19. Advantages Increase transferrins Increase IL–1 activity Disadvantages Tachycardia Acidosis Dehydration Fever

  20. The Complement System • Serum proteins activated in a cascade. Figure 16.9

  21. Effects of Complement Activation • Opsonization or immune adherence: Enhanced phagocytosis. • Membrane attack complex: Cytolysis. • Attract phagocytes. Figure 16.10

  22. Effects of Complement Activation Figure 16.11

  23. Classical Pathway Figure 16.12

  24. Alternative Pathway Figure 16.13

  25. Lectin Pathway Figure 16.14

  26. Some Bacteria Evade Complement • Capsules prevent C activation. • Surface lipid-carbohydrates prevent MAC formation. • Enzymatic digestion of C5a.

  27. Interferons (IFNs) • Alpha IFN and Beta IFN: Cause cells to produce antiviral proteins that inhibit viral replication. • Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria.

  28. Interferons (IFNs) Figure 16.15

  29. Transferrins Bind serum iron Antimicrobial peptides Lyse bacterial cells Innate Immunity

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