1. Non-Specific Defenses The first line against disease

2. Nonspecific Defenses of the Host SusceptibilityLack of resistance to a disease SusceptibilityLack of resistance to a disease Resistance Ability to ward off disease Resistance Ability to ward off disease Nonspecific resistanceDefenses against any pathogen Nonspecific resistanceDefenses against any pathogen Specific resistanceImmunity, resistance to a specific pathogen Specific resistanceImmunity, resistance to a specific pathogen

3. Host Defenses Figure 16.1

4. Skin Skin Epidermis consists of tightly packed cells with Keratin, a protective protein Epidermis consists of tightly packed cells with Keratin, a protective protein Mucous membranes Mucous membranes Ciliary escalator Ciliary escalator Microbes trapped in mucus are transported away from the lungs Microbes trapped in mucus are transported away from the lungs Lacrimal apparatus Lacrimal apparatus Washes eye Washes eye Saliva Saliva Washes microbes off Washes microbes off Urine Urine Flows out Flows out Vaginal secretions Vaginal secretions Flow out Flow out Mechanical Factors

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

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

7. Formed Elements In Blood Table 16.1

8. Percentage of each type of white cell in a sample of 100 white blood cells Percentage of each type of white cell in a sample of 100 white blood cells Differential White Cell Count Neutrophils60-70% Basophils0.5-1% Eosinophils2-4% Monocytes3-8% Lymphocytes20-25%

9. Neutrophils: Phagocytic Neutrophils: Phagocytic Basophils: Produce histamine Basophils: Produce histamine Eosinophils: Toxic to parasites, some phagocytosis Eosinophils: Toxic to parasites, some phagocytosis Monocytes: Phagocytic as mature macrophages Monocytes: Phagocytic as mature macrophages Fixed macrophages in lungs, liver, bronchi Fixed macrophages in lungs, liver, bronchi Wandering macrophages roam tissues Wandering macrophages roam tissues Lymphocytes: Involved in specific immunity Lymphocytes: Involved in specific immunity White Blood Cells

10. Phagocytosis Figure 16.8a

11. Microbial Evasion of Phagocytosis Inhibit adherence: M protein, capsules Inhibit adherence: M protein, capsules Streptococcus pyogenes, S. pneumoniae Kill phagocytes: Leukocidins Kill phagocytes: Leukocidins Staphylococcus aureus Lyse phagocytes: Membrane attack complex Lyse phagocytes: Membrane attack complexListeriamonocytogenes Escape phagosome Escape phagosomeShigella Prevent phagosome- lysosome fusion Prevent phagosome- lysosome fusionHIV Survive in phagolysosome Survive in phagolysosome Coxiella burnetti

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

13. Chemicals Released by Damaged Cells Histamine Histamine Vasodilation, increased permeability of blood vessels Kinins Kinins Vasodilation, increased permeability of blood vessels Prostaglandins Prostaglandins Intensity histamine and kinin effect Leukotrienes Leukotrienes Increased permeability of blood vessels, phagocytic attachment

14. Inflammation Figure 16.9a, b

15. Inflammation Figure 16.9c, d

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

17. Serum proteins activated in a cascade. Serum proteins activated in a cascade. The Complement System Figure 16.10

18. Effects of Complement Activation Opsonization or immune adherence: enhanced phagocytosis Opsonization or immune adherence: enhanced phagocytosis Membrane attack complex: cytolysis Membrane attack complex: cytolysis Attract phagocytes Attract phagocytes Figure 16.11

19. Effects of Complement Activation Figure 16.12

20. Classical Pathway Figure 16.13

21. Alternative Pathway Figure 16.14

22. Lectin Pathway Figure 16.15

23. Some bacteria evade complement Capsules prevent C activation Capsules prevent C activation Surface lipid-carbohydrates prevent MAC formation Surface lipid-carbohydrates prevent MAC formation Enzymatic digestion of C5a Enzymatic digestion of C5a

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

25. Figure 16.16 1 2 3 4 5 Viral RNA from an infecting virus enters the cell. The infecting virus replicates into new viruses. The infecting virus also induces the host cell to produce interferon on RNA (IFN-mRNA), which is translated into alpha and beta interferons. Interferons released by the virus-infected host cell bind to plasma membrane or nuclear membrane receptors on uninfected neighboring host cells, inducing them to synthesize antiviral proteins (AVPs). These include oligoadenylate synthetase, and protein kinase. New viruses released by the virus-infected host cell infect neighboring host cells. 6 AVPs degrade viral m-RNA and inhibit protein synthesis and thus interfere with viral replication.