BIOL-K 338 Lecture 4: Innate Immunity Notes

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Innate Immunity
Lecture 4
Review
o Blood Cells: leukocytes (neutrophils, lymphocytes, monocytes, eosinophils, basophils)
o Macrophage outside of blood, monocyte in blood
o NK cells: in tissues (lymphocytes but not really)
o Primary lymphoid: thymus (t cell maturation), bone marrow (b cell maturation)
o Secondary lymphoid: spleen, lymph nodes, MALT, GALT, BALT
o Lyph Fluid: aptured pathoges ad other leaks fro apillaries to atiate ells
(lymphocytes, dendritic, macrophages), moves w/ muscle use
Immunity
o Specific Mechanisms
Humoral (blood and lymph)
Antibody mediated, b-cell and t-cell
Cell mediated/cytotoxic
Cytotoxic t-cells and helper t-cells, DTH 9delayed type hypersensitivity), direct
cell contact
o Non-Specific
Innate immunity
Born with it (phagocytosis and inflammation)
Innate Immunity (Non-Specific)
o Inborn, non-adaptive defense mechanisms (phagocytosis)
o Always present and ready, rapid response, first line of defense
o Weak protection, non-specific (can damage host cells: collateral from inflammation)
Acquired Immunity (Specific)
o Develops in response to infection (recruited)
o Very powerful, essential in vertebrate, does not damage host cells/tissues
o Slow (week or so after infection develops)
Innate Immune System
o PAMPs: only on microbes (not in humans)
Pathogen associated molecular pattern
o DAMPs: damaged/death associated molecular pattern (necrotic or apoptotic cells)
o Self-Nonself: ignore own cells and attack damaged cells/pathogens
Perfect in innate, good in adaptive
o Memory responses: NONE in innate memory
o Major Cell Types
Innate: phagocytes, nk cells, leukocytes
Adaptive: lymphocytes, antigen presenting cells, MHC I cells and MHC II Professional
APC cells
Pathogen
o Infection agents that can cause disease
o Innate responses prevent establishment of many infections
o Infectious diseases occur when initial innate responses fail to contain pathogen
Adaptive immune response required for infection
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First Line of Defense (defense at epithelial surface)
o Integrity of epithelial cell barrier: loss of integrity as result of wound can lead to infection
o Removal of pathogens via ciliary movement of mucus
Move pathogens out and trap
Cystic fibrosis: thicker mucus cannot be cleared by cilia (bacteria in lung = infection)
o Production of Antimicrobial Peptides (histatins, alpha-defensis, beta-defensins)
Chroh’s disease: assoiated / dereased defesig produtio i itestie
o Production of surfactant proteins in lung (coat and opsonize)
Opsonize: facilitate phagocytosis, coat to trigger immune response (pepper for taste)
o Production of antimicrobial proteins
Lysosome (opsonizing enzyme) and lactoferrin (iron-binding) in secretions
o Maintenance of nonpathogenic (microbiota) flora
Antibiotic-associated colitis: antibiotics kill normal intestinal flora
Can lead to overgrowth of clostridium difficile (fecal transplant needed)
Barrier: Innate Immunity
o Chemical gradient (slightly acidic) and antimicrobial proteins/peptides in skin
o Pathogen enters: infects cell and killed by NK cell or binds to cells and activates cytokines
(inflammation) and releases antimicrobials
Macrophage/dendritic cell activates adaptive immune response
Psoriasin inhibits gram negative bacteria from colonizing
o Staph will grow (gram positive)
Second Line of Defense: phagocytosis by macrophages and neutrophils
o Macrophages are first responders, first to encounter pathogen across epithelial surface
o Neutrophils recruited to site shortly after as result of tissue wounding, complement activation,
or secretion of chemotactic factors by macrophages at site
o Macrophages and neutrophils phagocytose bacteria expressing PAMP/DAMP
Reogized y PRR’s patter reogitio reeptor o arophage/eutrophil surfae
PRP recognizes PAMP/DAMP, but not attached to cell itself
Can recognize opsonins (antibody, complement C3b, or c-reactive proteins)
Complement components: travels inactivated through blood in parts A and B
o C3B (active) attaches to surface of antigen to activate opsinin
LOTS of receptors for Phagocytosis
o PRRs, Opsonins, complements, etc
PRR’s o arophage/eutrophil Recognize PAMPs
o Can be destroyed by antimicrobial
o Phagocytes recognized and taken to be degraded by lysosome
o Can be opsonized and complement destroys
o Can be opsonized and enhance phagocytosis and dendritic cells in lymph, initiate t-cell response
Gram Negative Bacteria
o Has 2 membranes
o Peptidoglycan is protective (thinner than in positive membrane) between 2 membranes
o Endotoxic LPS: attached to surface of pathogen and causes problems
Gram Positive Bacteria
o 1 membrane and outer peptidoglycan layer
o Treated due to exposed peptidoglycan layer and glycolipids (not endotoxins: PAMPs)
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