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Body Defenses

Body Defenses. Body Defenses. The body has two defense systems for foreign materials: Innate (nonspecific) defense system = immediately protects against a variety of invaders Adaptive (specific) defense system = specific defense is required for each type of invader

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Body Defenses

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  1. Body Defenses

  2. Body Defenses • The body has two defense systems for foreign materials: • Innate (nonspecific) defense system = immediately protects against a variety of invaders • Adaptive (specific) defense system = specific defense is required for each type of invader • Immunity—specific resistance to disease

  3. Immune System Figure 12.6

  4. Innate Defense System First Line of Defense = Surface membrane barriers • Skin and mucous membranes • Physical barrier to foreign materials • Also provide protective secretions • pH of the skin is acidic to inhibit bacterial growth • Sebum is toxic to bacteria • Vaginal secretions are very acidic

  5. Stomach mucosa • Secretes hydrochloric acid • Has protein-digesting enzymes • Saliva and lacrimal fluid contain lysozymes, an enzyme that destroy bacteria • Mucus traps microogranisms in digestive and respiratory pathways

  6. Innate Body Defenses Table 12.1 (1 of 2)

  7. Second Line of Defense: Cells and Chemicals • Phagocytes • Natural killer cells • Inflammatory response • Antimicrobial proteins • Fever

  8. Phagocytes • Example: macrophages • Engulf foreign material into a vacuole • Enzymes from lysosomes digest the material

  9. Microbe adheres to phagocyte (b) Figure 12.7b, step 1

  10. Microbe adheres to phagocyte Phagocyte engulfs the particle (b) Figure 12.7b, step 2a

  11. Microbe adheres to phagocyte Phagocyte engulfs the particle Phagocytic vesiclecontaining microbeantigen (phagosome) Lysosome (b) Figure 12.7b, step 2b

  12. Microbe adheres to phagocyte Phagocyte engulfs the particle Phagocytic vesiclecontaining microbeantigen (phagosome) Lysosome Phagocytic vesicle isfused with a lysosome Phagolysosome Lysosomalenzymes (b) Figure 12.7b, step 3

  13. Microbe adheres to phagocyte Phagocyte engulfs the particle Phagocytic vesiclecontaining microbeantigen (phagosome) Lysosome Phagocytic vesicle isfused with a lysosome Phagolysosome Microbe in fused vesicleis killed and digested bylysosomal enzymes withinthe phagolysosome Lysosomalenzymes (b) Figure 12.7b, step 4

  14. Microbe adheres to phagocyte Phagocyte engulfs the particle Phagocytic vesiclecontaining microbeantigen (phagosome) Lysosome Phagocytic vesicle isfused with a lysosome Phagolysosome Microbe in fused vesicleis killed and digested bylysosomal enzymes withinthe phagolysosome Lysosomalenzymes Indigestible andresidual materialis removed byexocytosis (b) Figure 12.7b, step 5

  15. Natural killer (NK) cells • Can lyse (disintegrate or dissolve) and kill cancer cells • Can destroy virus-infected cells http://www.youtube.com/watch?v=HNP1EAYLhOs

  16. Inflammatory response • Triggered when body tissues are injured • 4 signs of acute inflammation: • Redness, Heat, Swelling, Pain • Steps: • Injured cells releasing inflammatory chemicals = histamine and kinins • Causes blood vessels to dilate & capillaries to become leaky • Activates pain receptors 2. Phagocytosis • Neutrophils (= WBC) : • Move by diapedesis • Use chemotaxis to locate damaged tissue and/or pathogens • Clean up the tissue • Monocytes become macrophages and complete disposal of cell debris

  17. Positivechemotaxis 4 Inflammatorychemicals diffusingfrom the inflamedsite act as chemotacticagents Neutrophils 1 Enter blood frombone marrow Diapedesis 3 Cling tovascular wall 2 Endothelium Capillary wall Basal lamina Figure 12.9

  18. Inflammatorychemicals diffusingfrom the inflamedsite act as chemotacticagents Neutrophils 1 Enter blood frombone marrow Figure 12.9, step 1

  19. Inflammatorychemicals diffusingfrom the inflamedsite act as chemotacticagents Neutrophils 1 Enter blood frombone marrow Cling tovascular wall 2 Endothelium Capillary wall Basal lamina Figure 12.9, step 2

  20. Inflammatorychemicals diffusingfrom the inflamedsite act as chemotacticagents Neutrophils 1 Enter blood frombone marrow Diapedesis 3 Cling tovascular wall 2 Endothelium Capillary wall Basal lamina Figure 12.9, step 3

  21. Positivechemotaxis 4 Inflammatorychemicals diffusingfrom the inflamedsite act as chemotacticagents Neutrophils 1 Enter blood frombone marrow Diapedesis 3 Cling tovascular wall 2 Endothelium Capillary wall Basal lamina Figure 12.9, step 4

  22. Slide 2 Figure 12.8  Flowchart of inflammatory events. Injurious agents

  23. Slide 3 Injurious agents Cells damaged

  24. Slide 4 Injurious agents Cells damaged Release kinins, histamine,and other chemicals

  25. Slide 5 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate

  26. Slide 6 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Increased bloodflow into area

  27. Slide 7 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Increased bloodflow into area Redness Heat

  28. Slide 8 . Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Increased bloodflow into area Redness Heat Brings morenutrients andoxygen to area Increasesmetabolicrate oftissue cells

  29. Slide 9 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Increased bloodflow into area Redness Heat Brings morenutrients andoxygen to area Increasesmetabolicrate oftissue cells

  30. Slide 10 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Increased bloodflow into area Edema (fluid intissue spaces) Redness Heat Pain Swelling Brings morenutrients andoxygen to area Increasesmetabolicrate oftissue cells

  31. Slide 11 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Increased bloodflow into area Edema (fluid intissue spaces) Redness Heat Pain Swelling Brings morenutrients andoxygen to area Increasesmetabolicrate oftissue cells Possibletemporarylimitation ofjoint movement

  32. Slide 12 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Clottingproteinsenter area Increased bloodflow into area Edema (fluid intissue spaces) Redness Heat Pain Swelling Brings morenutrients andoxygen to area Increasesmetabolicrate oftissue cells Possibletemporarylimitation ofjoint movement

  33. Slide 13 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Clottingproteinsenter area Increased bloodflow into area Edema (fluid intissue spaces) Redness Heat Pain Swelling Brings morenutrients andoxygen to area Fibrinbarrier Increasesmetabolicrate oftissue cells Possibletemporarylimitation ofjoint movement

  34. Slide 14 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Neutrophils and thenmonocytes(and other WBCs)enter area Clottingproteinsenter area Increased bloodflow into area Edema (fluid intissue spaces) Redness Heat Pain Swelling Brings morenutrients andoxygen to area Fibrinbarrier Increasesmetabolicrate oftissue cells Possibletemporarylimitation ofjoint movement

  35. Slide 15 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Neutrophils and thenmonocytes(and other WBCs)enter area Removal ofdamaged/deadtissue cells andpathogensfrom area Clottingproteinsenter area Increased bloodflow into area Edema (fluid intissue spaces) Redness Heat Pain Swelling Brings morenutrients andoxygen to area Fibrinbarrier Increasesmetabolicrate oftissue cells Possibletemporarylimitation ofjoint movement

  36. Slide 16 Injurious agents Cells damaged Release kinins, histamine,and other chemicals Blood vesselsdilate Capillariesbecome “leaky” Neutrophils and thenmonocytes(and other WBCs)enter area Removal ofdamaged/deadtissue cells andpathogensfrom area Clottingproteinsenter area Increased bloodflow into area Edema (fluid intissue spaces) Redness Heat Pain Swelling Brings morenutrients andoxygen to area Fibrinbarrier Increasesmetabolicrate oftissue cells Possibletemporarylimitation ofjoint movement Healing

  37. Antimicrobial proteins • Attack microorganisms and/or hinder their ability to reproduce • Complement proteins • Activated when they encounter and attach to foreign cells’ surfaces (= complement fixation) • Form membrane attack complexes (MAC) that make holes in membrane so that water rushes in and cell bursts • Release vasodilators and chemotaxis chemicals, cause opsonization (=makes foreign cell membrane sticky to make phagoctosis easier) • Interferon • Proteins secreted by virus-infected cells • Bind to healthy cell surfaces to interfere with the ability of viruses to multiply

  38. Figure 12.10

  39. Fever • Abnormally high body temperature • Hypothalamus heat regulation can be reset by pyrogens (secreted by white blood cells) • High temperatures stop the release of iron and zinc from the liver and spleen needed by bacteria • Fever increases the speed of tissue repair

  40. Summary of Nonspecific Body Defenses Table 12.1 (2 of 2)

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