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Chapter 16

Chapter 16. Nonspecific Defenses of the Host. Nonspecific Defenses of the Host. Susceptibility Lack of resistance to a disease Resistance Ability to ward off disease Nonspecific resistance Defenses against any pathogen

bethany-watts
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Chapter 16

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  1. Chapter 16 Nonspecific Defenses of the Host

  2. 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

  3. Host Defenses Figure 16.1

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

  5. 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

  6. Chemical Factors • fatty acid in sebum • Low pH (3-5) of skin • Lysozyme in 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

  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, some phagocytosis • Monocytes: Phagocytic as mature macrophages • Fixed macrophages in lungs(alveolar), liver (kupffer), bronchi • Wandering macrophages roam tissues • Lymphocytes: Involved in specific immunity

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

  12. Phagocytosis Figure 16.8a

  13. Microbial Evasion of Phagocytosis

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

  15. Chemicals Released by Damaged Cells

  16. Inflammation Figure 16.9a, b

  17. Inflammation Figure 16.9c, d

  18. 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)

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

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

  21. Effects of Complement Activation Figure 16.12

  22. Classical Pathway Figure 16.13

  23. CYTOLYSIS • Antibody recognize and attached antigen, • The complement C1 bind to two or more adjacent antibodies and activated. • C1 activated C2 and C4 by split C2 to C2a and C2b and C4 to C4a and C4b. • C2a and C4b bind to form another enzyme that activate C3 by splitting into two fragment C3a and C3b. • C3b initiates a sequence of reactions involve C5-C9 that called membrane attack complex. • the activated proteins make transmembrane channels in the invading cell lead to loss of ions and cytolysis. • This process called complement fixation.

  24. INFLAMMATION • C3a and C5a contribute in acute inflammation. • C3a and C5a bind to mast cells, basophiles, and blood platelets to trigger the release histamine which a powerful chemotactic attract phagocytes to site of complement fixation.

  25. OPSONIZATION • When bound to the surface of a microorganisms . • C3 can interact with special receptors on phagocytes to promote phagocytosis.

  26. Alternative Pathway Figure 16.14

  27. Lectin Pathway • The lectin pathway is mediated by circulating proteins called mannan-binding lectin (MBL) - also known as mannan-binding protein (MBP). • MBL binds to mannose-rich glycans . • Activation of the lectin pathway begins when mannan-binding lectin (MBL) binds to the mannose groups of microbial carbohydrates.

  28. Lectin Pathway • Two more lectin pathway proteins called MASP1 and MASP2 (equivalent to C1r and C1s of the classical pathway) now bind to the MBL . • This forms an enzyme similar to C1 of the classical complement pathway that is able to cleave C4 and C2 to form C4bC2a, enzymatically splitting molecules of C3 into C3a and C3b.

  29. Lectin Pathway Figure 16.15

  30. Interferons (IFNs) • Small protein with MW 15000-30000. • Alpha IFN & Beta IFN: Cause cells to produce antiviral proteins that inhibit viral replication • Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria

  31. Interferons (IFNs) 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

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