Innate Immunity: Nonspecific Defenses of the Host

1. 16 Innate Immunity: Nonspecific Defenses of the Host

2. TERMINOLOGY • 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.

3. Host Defenses: OR WHAT WE ARE BORN WITH OR THE ABILITY TO MAKE THEM Figure 16.1

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

5. 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

6. 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.

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

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

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

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

11. White Blood Cells • Neutrophils: Phagocytic • Basophils: Produce histamine • Eosinophils: Toxic to parasites and some 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. PLAY Animation: Host Defenses

12. 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

13. Phagocytosis Figure 16.7

14. Microbial Evasion of Phagocytosis PLAY Animation: Phagocytosis

15. Inflammation • 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

16. Chemicals Released by Damaged Cells

17. Inflammation Figure 16.8a–b

18. Inflammation PLAY Animation: Inflammation Figure 16.8c–d

19. 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).

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

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

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

23. Effects of Complement Activation Figure 16.11

24. Classical Pathway Figure 16.12

25. Alternative Pathway Figure 16.13

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

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