Nonspecific Defenses of the Host

1. Nonspecific Defenses of the Host • Susceptibility Lack of resistance to a disease • Resistance Ability to ward off disease • Nonspecific resistance Defenses against any pathogen • Specific resistance Immunity, resistance to a specific pathogen

2. Host Defenses Figure 16.1

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

4. Mechanical 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

5. Chemical Factors • Fungistatic fatty acid in sebum • Low pH (3-5) of skin • Lysozyme in perspiration, tears, saliva, and tissue fluids • Low pH (1.2-3.0) of gastric juice • Transferrins in blood find iron

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

7. Formed Elements In Blood Table 16.1

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

9. Phagocytosis • Phago: eat • Cyte: cell • Ingestion of microbes or particles by a cell, performed by phagocytes

10. Phagocytosis Figure 16.8a

11. Microbial Evasion of Phagocytosis

12. Inflammation • Redness • Pain • Heat • Swelling (edema) • Acute Inflammation • Chronic Inflammation

13. Inflammation • Acute-phase proteins activated (complement, cytokine, kinins) • Vasodilation (histamine, kinins, prostaglandins, leukotrienes) • Margination and emigration of WBCs • Tissue repair

14. Chemicals Released by Damaged Cells

15. Inflammation Figure 16.9a, b

16. Inflammation Figure 16.9c, d

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

18. The Complement System • Antimicrobial Serum proteins that are a component of the inflammatory response. • Normally Inactive. • Activated in a cascade. • C3 is involved in all cases. Figure 16.10

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

20. Inflammation May be Stimulated by Complement Phagocyte Chemotaxis Degranulation of a Mast Cell Figure 16.12

21. Complement Activation: Classical Pathway Figure 16.13

22. Alternative Pathway Figure 16.14

23. Lectin Pathway Figure 16.15

24. Some bacteria evade complement • Capsules prevent Complement activation • Surface lipid-carbohydrates prevent MAC formation • Enzymatic digestion of C5a

25. Interferons (IFNs) • Component of Host defense against Viral Infection • Alpha IFN & Beta IFN: Cause cells to produce antiviral proteins that inhibit viral replication • Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria

26. IFN alpha and IFN beta New viruses released by the virus-infected host cell infect neighboring host cells. 5 The infecting virus replicates into new viruses. 2 AVPs degrade viral m-RNA and inhibit protein synthesis and thus interfere with viral replication. 6 Viral RNA from an infecting virus enters the cell. 1 The infecting virus also induces the host cell to produce interferon on RNA (IFN-mRNA), which is translated into alpha and beta interferons. 3 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. 4 Figure 16.16