Innate Immunity

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Innate Immunity
2015-04-19 20:13:01

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  1. Host defenses
    1. Innate (nonspecific)

    2. Acquired (specific)
  2. Innate
    1. First line of defense

    2. Second line of defense
  3. First line of defense
    a surface protection composed of anatomical and physiological barriers that keep microbes from penetrating sterile body compartments
  4. First line of defense 2
    • 1. Physical barriers
    • 2. Chemical barriers
    • 3. Genetic barriers
  5. Innate 2
    Response time: 1st responder

    Recognizes pathogens by predetermine patterns; toll-like receptors (TLR's)

    No memory
  6. Adaptive
    Response time: 2nd to respond, clears infection

    Learns each pathogen individually as it’s encountered

    Memory to previously encountered pathogens
  7. Physical barriers to prevent microbial entry
    • 1. Skin (line of defense)
    •      •Keratin
    •      •Epithelial cells tightly packed
    •      •Sebum

    • 2. Mucous membranes
    •      •Layer of epithelial cells
    •      •Secrete mucous
    •      •GI, GU, & Respiratory Tract
  8. Chemical defenses: Flushing mechanisms
    Non specific

    1.Lacrimal Apparatus: tears


    3.Cilary Escalator

    4.Perspiration: lysozyme



  9. Genetic Defenses
    Genetic differences in susceptibility can exist within members of one species.
  10. Normal microbiota = normal flora
    Organisms that are considered normal to be present

    • What do they do? 
    • 1. Competitive exclusion
    • 2. Microbial antagonism
  11. Competitive exclusion
    • they produce harmful waste products, they take up space, they take nutrients, they
    • can alter the pH, etc
  12. Microbial antagonism
    • the normal microbiota has
    • an ability to kill or injure a different microbe -due to a property your normal flora has
  13. Second Line of Defense
    Cells of the Innate Immune System
  14. Cells of the Innate Immune System
    • 1.Hematopoiesis
    • 2. Stem Cells
    • 3. Blood cells
  15. Hematopoiesis
    refers to production of blood cells from stem cells
  16. Stem cell
    an immature cell that can differentiate into specialized cells (stem cell = undifferentiated cell)
  17. Types of blood cells
    1. RBC’s / Erythrocytes

    2. Platelets – regulates blood clotting when there is injury

    3. WBC’s - referred to as Leukocytes

    4. Granulocytes

    5. Agranulocytes
  18. primary lymphoid organs
    are the site of lymphocyte maturation where t-cells and b-cells mature.

    occurs in the bone marrow and the thymus
  19. secondary lymphoid organs
    -are the locations where the lymphocytes will meet the pathogen - sort of the command center 

    -the lymphnodes and spleen
  20. The Lymphatic System
    •Lymphatic vesicles

    •Primary lymphoid organs

    •Secondary lymphoid organs
  21. Innate Immune Cells
    • – Neutrophils 
    • – Monocytes
    • – Basophils 
    • – Macrophages
    • – Eosinophils 
    • – NK Cells
  22. What do the innate immune cells do



    • –Antimicrobial substances such as Complement
    •      •Complement

  23. How does the innate immune system recognize pathogens?
    • there are toll like receptors on the surface of cells. they are single membrane receptor protein. nonspecifically help us interact with bacteria when it does this it activates other things to occur such as production of various interleukin. *Toll like markers that can
    • nonspecifically interact with pathogens.
    • When the TLR4 recognizes and interacts with the LPS of a gram negative bacteria its going to signal other molecules such as cytokines and interleukins to come into play
  24. Phagocytosis
    Phagocytes engulf & destroy microbes

    • -The two main types of white blood cells involved in phagocytosis:
    • • Neutrophils
    • • Macrophages
  25. Neutrophils
    • - They squeeze through your capillaries to control tissue to help clear up infections
    • - made in the bone marrow
    • - Make up about 60% of the wbc’s
    • - travel through the blood and are shortlived
    • - Effective
    • - Released in large quantities during infection
    • - Dead neutrophils is pus
  26. Macrophages
    • - made in bone marrow
    • - when traveling in the blood we refer to it as monocytes
    • - Longer lived than neutraphils and larger

    Macrophages will cut up the pathogen and display the pathogen on their surface and then lymphocyte will come and recognize that.
  27. Phagocytosis and Phagolysosome
    • when the bacteria is engulfed by a phagocyte it will be contained in a vacuole. the phagocyte has little vacuoles that contain lysosomes which has lytic enzymes.
    • phagolysosome = where the lysosome will fuse with the phagosome.
    • the phagosome contains the bacteria. lysosome then destroys the bacteria and then eject the debris. phagolysosome can take 10 - 30 minutes to kill the bacteria.
  28. Evasion of Phagocytosis
    1.Block adherence

    2.Escape to the cytoplasm

    • 3.Block fusion of the phagosome
    • & lysosome
  29. Why do we get sick?
    - Various microorganisms have various ways of avoiding phagolysosome

    - Tuberculosis prevents phagolysosome; resides in and infects the macrophages

    • - Some bacteria can escape to the cytoplasm
    • to escape being engulfed.

    - Some can also kill the phagocyte
  30. Inflammation
    4 signs of inflammation - Redness, Warmth, swelling, and Pain

    - Acute inflammation - intense but shortlived

    - Chronic inflammation - not as intense but carried out over a long period of time
  31. 3 stages of inflammation
    1.Vasodilation & increased permeability of blood vessels (wbc’s go in)

    • 2.Phagocyte migration & phagocytosis - how can they get there? with vasodilation &
    • increased permeability of the blood.

    3.Tissue repair
  32. Inflammation 2
    Step 1 - Vasodialation

    • • Histamine
    • • Kinins 
    • • Prostaglandins
    • • Leukotrines
  33. Histamine
    contributes to inflammatory response & causes constriction of smooth muscle
  34. Kinins
    proteins in blood that affect BP and attract phagocytic granulocytes to injured area
  35. Prostaglandins
    • Hormone-like substance plays part in inflammation.  Intensify effect of histamine & kinins. Help phagocytes move through capillary
    • walls. First discovered in the prostate
  36. Leukotrines
    produced by mast cells. Contribute to most features during allergic reaction
  37. Increased permeability of venule during inflammation
    Has interstitial spaces

    More fluid and antimicrobial chemicals

    Diapedesis - Monocytes squeeze through interstitial space
  38. Permeability
    • expansion in the vessels and with expansion you can allow things to come out and patrol.
    • For example platelets and monocytes
  39. What makes blood vessels more permeable?
    Prostaglandins and leukotrines
  40. What does histamine cause
    vasodilation, increasing blood flow to the site of a cut
  41. Macrophages and neutrophils
    squeeze through walls of blood vessels (diapedesis)
  42. Increased permeability allows
    antimicrobial chemicals and clotting proteins to see into damaged tissue but also results in swelling, pressure on nerve endings, and pain
  43. What migrates to damaged tissue site
    Phagocytes migrate to the site and devour bacteria
  44. What repairs damaged tissue
    Undifferentiated stem cells repair the damaged tissue
  45. Outcome of Inflammation
    Overall Goal:  Repair damaged site
  46. Problems with inflammation
    –Bystander damage: you generally want inflammation but for some things like spinal injury it causes more damage

    –Septic shock: blood poisoning
  47. Fever
    Definition: increase in internal body temperature to levels that are above normal 

    It is a systemic Response to Infection

    Caused by: Infection from bacteria, their toxins or viruses.
  48. Antimicrobial Substances
    • Complement (C’) - Complement protein is
    • found in the blood

    Made by leukocytes to kill microbes – nitric oxide (NO), superoxide, hydrogen peroxide, defensins, transferrins, interferons
  49. Antimicrobial Substances 2
    –some cytokines have antimicrobial properties (ex. interferons) but in general are molecules released from leukocytes to communicate with other cells and coordinate immune responses
  50. Complement
    • 30 proteins made by the liver which
    • circulate in the blood and are only functional when activated

    Activation is a cascade of ordered interactions between these proteins
  51. Outcomes of complement activation
    1.Lysis of the microbe

    2.Increased inflammation

    3.Increased phagocytosis through opsonization
  52. Complement system - Classical pathway
    • 1) Antibody binds to bacteria
    • 2) C1 binds to Ab
    • 3) C1 cleaves C4 & C2
    • 4)C4b C2b binds and cleaves C3
    • 5) C4b C2b C3b binds and cleaves C5
    • 6) C5b binds C6, C7, C8
    • 7) C5b C6 C7 C8 bind many molecules of C9
    • creating a hole in the bacteria cell membrane
    • lysing the cell. This is the membrane attack
    • complex
  53. Alternate pathway
    -Does not involve antibody.

    -c3 binds directly to proteins on the pathogen

    -Does not have c1, c2, c4.

    -It begins with c3
  54. Lectin Pathway
    •Mannose-binding lectin (MBL) also released from the liver

    •Binds to microbe to trigger series of events
  55. Cytolysis
    lysis of the cell

    • Occurs through MAC that occurs when c5b
    • binds to c6 c7 c8 c9 to form MAC that lysis the cell
  56. Inflammation (complement system)
    Increasepermeability of the blood vessel due to c3a or c5a
  57. Increase phagocytosis through opsonization 2
    • where c3b binding on the surface of the bacteria so that it draws the phagocyte towards it to be
    • engulfed.
  58. degranulization
    • c3a and c5a bind to a mast cell causing degranulization. This degranulization is
    • evident by the result of the release of histamine which causes inflammation
  59. Interferon – Antiviral Cytokines
    •IFN-a & IFN-b: cause cells to degrade mRNA to block protein synthesis in an attempt to halt viral replication
  60. Interferon – Antiviral Cytokines 2
    •IFN-y: Activates neutrophils and macrophages to kill microbes by causing:

    –Increased phagocytosis

    • –Increased production of antimicrobial molecules such as NO, hydrogen peroxide, &
    • superoxide
  61. Interferon – Antiviral Cytokines 3
    • Major role in controlling acute illness,
    • ex. colds & flu

    • Side effects: nausea, fatigue, headache,
    • vomiting, weight loss, & fever