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Unformatted text preview: Chapter 2 Review of innate immunity- NK cells, granulocytes, mast cells, dendritic cells o Recognize LPS, Virally infected cells Pathogen patterns o Immediate response o Cytokines Infection and response divided into a series of stages- local immune response either stops or contains infection, carries infectious agents to lymph nodes The First Line of Defense intrinsic barriers- Intrinsic epithelial barriers of infection skin, guy epithelium, mucous membranes. Tight junctions within the cells. - Mechanical - Blow of air preventing deposition of bacteria/viruses in lungs, movement of mucus by cilia- Chemical pH, enzymes, etc- Microbiological normal bacteria Chemical defenses- Enzymes lysozymes, phospholipaseA, digestive enzymes, bile salts all inhibit microbial growth- Low pH in stomach, skin- Peptides alpha/beta degensins, cryptidins damage bacterial cell membranes- Surfectants lung, inhibit microbial growth 1) Receptors for pathogens on neutrophils. Triggering of cell surfaces leads to increased phagocytosis Macrophages- Macrophages derived from circulating monocytes. Express receptors for bacterial components, including mannose and glucan receptors, LPS receptors, and Toll-like receptors. Binding of bacteria to macrophage stimulates phagocytosis and uptake of pathogens into intracellular vesicles.- Macrophage expresses receptors for many bacterial constituents bacteria binding to receptors initiates release of cytokines and lipid mediators of inflammation macrophages engulf and digest bacteria Phagocyte defenses- Acidification lowering of pH- Toxic oxygen products free radicals, superoxides, hydroxy radicals- Toxis nitrous oxides NO, also damaging- Antimicrobial peptides defensins and cationic proteins- Enzymes lysozymes, acid hydrolases- Competitors Lactoferrin, B12-binding protein Mechanism for Reactive Oxide development- Respiratory burst in macrophages and neutrophils is caused by a transient increase in O2 consumption during production of oxygen metabolites- NADPH oxidase enzyme converts O2 to O2-, sometimes called respiratory burst- Superoxide dismutase converts superoxide into hydrogen peroxide to hypochlorite and hydroxyl radicals Peroxidase enzymes and iron further convert the hydrogen peroxide to hypochlorite ions and hydroxyl radicals Macrophage killing mechanisms 1) phagocytosis 2) Acidification 3) Production of ROS 4) Nitric Oxide Inflammation- Delivery of WBC and chemicals, Formation of physical barrier to prevent infection from spreading, Promotion of repair. 1) Redness and heat comes from dilation of blood vessels caused by cytokines from macrophages 2) Leukocytes move to periphery of blood vessel as a result of increased expression of adhesion molecules (extravasation) 3) Leukocytes extravasate at site of infection - Edema 4) Blood clotting occurs in the microvessels Extravasation - Monocyte binds adhesion molecules on vascular endothelium near sites of infection and gets chemokine...
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This note was uploaded on 04/17/2008 for the course BIO 4750 taught by Professor Leavey during the Spring '08 term at Georgia Institute of Technology.
- Spring '08