MMI 301-Exam 2-Lecture 9: Innate Immunity

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MMI 301-Exam 2-Lecture 9: Innate Immunity
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MMI 301 Exam 2 Lecture 9
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  1. Components of Anatomical Barriers
    • -Skin,
    • tears, saliva, mucus, cilia in intestines/respiratory tracts
  2. Components of Humoral Barriers
    • -Acute
    • phase response, component system
  3. Components of Cellular Barriers
    • -Mast cells, dendritic cells,
    • macrophages, NK cells, neutrophils, eosinophils, basophils, granulocytes
  4. Mechanical Removal of Bacteria
    • -Beating
    • cilia- respiratory tract, fallopian tubes, middle ear

    •                                 -Flushing- Eyes,
    • urinary tract, intestines

    •                                 -Peristalis-
    • Intestines
  5. Harsh Enviroments for Bacteria
    • -Low pH-
    • Stomach/vagina

    •                                 -Surfactants-
    • Bile salts (made in liver, go to intestines)

    •                                 -Low iron-
    • Transferrin/lactoferrin bind free iron, Calprotectin bind zinc and manganese
  6. Lysozyme
    • :in
    • tears/salvia/sweat/respiratory secretions/cervical secretions

    •                                                 -Degrades
    • peptidoglycan/lysis bacteria

    •                                                 -Break
    • bounds between the sugars of the backbone
  7. Lactoperoxidase
    • :Saliva and
    • milk

    •                                                 -Catalyzes
    • production of H2O2, oxidative killing of bacteria
  8. Myeloperoxidase
    • :neutrophil
    • granules

    •                                                 -Catalyzes
    • production of hypochlorous acid (HOCL), oxidative killing of bacteria
  9. Digestive enzymes
    • :Mouth,
    • stomach, intestines

    •                                                 -Enzymes
    • including lipases and proteases

    •                                                 -Cause
    • cell lysis through degradation of membrane proteins/phospholipids
  10. Acute Inflammation
    • -If infectious
    • agents get through physical barrier, acute inflammation kicks in

    •                                 -Initial
    • response of host to harmful stimuli

    •                                 -Acute
    • inflammation contains infection

    •                                                 -Prevents
    • spread

    •                                                 -Capillary
    • expansion, increased blood flow (rash/warmth)

    • -Increased microvasculature
    • permeability, escape of proteins, leukocytes (macrophages) (edema)

    • -Leukocytes exit from capillaries to
    • infection site (pus)

    •                                                 -Inflammation leads to acute
    • phase response, activates complement cascade
  11. Acute Microbial Response
    • -Produces
    • molecules that bind bacteria, but not cells

    • -Produced in liver cells in response
    • to Il-1/Il-6/TNF released by macrophages in response to PAMP binding (such as
    • LPS), by PRRs

    • -Include C-reactive protein (CRP),
    • mannose-binding protein (MBP) and fibrinogen
  12. CRP/MBP
    • -CRP/MBP
    • serve as soluble pattern recognition receptors

    •                                                 -Recognizes
    • things on bacteria, but not host

    •                                                                 -Can
    • be opsonin

    •                                                                 -Can
    • activate the classical complement

    • -MBP binds mannose residues on
    • bacterial cell surfaces common to forms of LPS/capsules.

    • -Like CRP, MBP can be opsonin, can
    • also activate the lectin complement pathway
  13. Three Types of Complement Pathway
    • -Classical:
    • triggered by antibody
    • -Lectin:
    • Initiated by mannose-binding protein
    • -Alternative:
    • initiates directly on pathogen surface
  14. Consequences of Complement Activation
    • -Opsonization of pathogens
    • -Recruitment of inflammatory cells
    • -Direct killing of pathogens
  15. Complement Cascade of Lectin Pathway
    -Mannan-binding lectin->C4b->C3b->C3a->C5a->C5b6789
  16. Membrane Attack Complex Pathway
    • -C5b binds
    • C6 and C7
    • -C5b67 complexes bind to membrane via C7
    • -C8 binds complex and inserts into cell membrane
    • -C9 molecules bind complex and polymerize
    • -1-16 molecules bind to form a pore in membrane
  17. Complement Antibacterial Responses
    • -Alternative and Lectin pathways activated by bacterial surfaces
    • -Classic pathway activated by antibody-antigen complexes
    • -Production of chemotactic/anaphylotoxic proteins (C3a, C5a)
    • -Opsonization of bacteria (C3b)
    • -Promotion of killing of gram-neg bacteria by terminal complement lytic structure
  18. Discoverer of Phagocytosis
    Metchnikoff Starfish-Stabber
  19. Neutrophils
    • -Most abundant leukocytes in mammals
    •  -One of first responders in acute phase of inflammation
    • -Recruit/activate other cells by expressing and releasing cytokines
    • -Attack microorganism by:
    •        -Phagocytosis
    •        -Nuclear extracellular
    •        -Antimicrobial peptides
  20. Dendritic Cells
    • -Often in contact with externalenvironment                                                    -Skin,lungs, lining of GI
    • -Ideally placed to encounter extrinsic
    • antigens, including those expressed by invading pathogens
    • -Continuously sample surrounding/ingest antigens by endocytosis
    • -Important in presenting antigens to cells of the adaptive immune system
  21. Macrophages
    • -Important antibacterial phagocytic cell
    • -Kill by same mechanisms identical to neutrophils
    • -Production of IL-1, IL-6, and IL-12, TNF-α/TNF-β and interferon-α
    • -Presentation of antigen to CD4 T cell

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