BIOL 209 1st Edition Lecture 28 Outline of Last Lecture I. Question/Answer’sII. LymphocytesIII. InflammationIV. AllergyV. AdhesionVI. MultiplicationVII. ExozymesOutline of Current LectureI. Question/Answer’sII. ToxinsIII. Immune Evasion MechanismsCurrent LectureI. Question/Answer’sA. The toxin produced by vibrio cholera acts on the intestinal epithelium is an example of an: enterotoxinB. Which is not an immune mechanism that directly targets extracellular pathogens? CD8+ T cellsC. What immune mechanisms would be effective against Listeria? CD8+ T cellsII. ToxinsA. Produced by infectious bacteria can alter normal host cell function or kill cells – systematically or totallyB. Exozymes1. Work outside the cellC. Exotoxins1. Particularly secreted to act on host cells – generate endotoxins – either single monomers or A-B toxinsa. Kill: cytotoxinsb. Alter function: enterotoxins, neurotoxins, superantigensD. Endotoxins1. Released primarily upon pathogen lysis – LPS2. AB toxins are made of 2 subunits a. B subunit that binds the host cell surface and helps transport the A subunit3. Cytotoxins can also kill host cells by disrupting membranesThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.a. Example: hemolysins lyse erythrocytes – they clear around colonies on blood agar plate – it forms pores in host cells and reside in membranes4. Enterotoxins affect cell function of intestinal epithelial cellsa. Cholera toxin (secreted A-B toxin) activates ion pumps causing secretion out of intestinal cells- Massive loss of water5. Superantigens alter function of cell by stimulating (and possibly killing) T cells to produce cytokinesa. Provide cross-bridge between MHC and T cellb. Large proportion of T cells respond to superantigen c. Induce massive production of cytokines- Which can eventually kill T cells6. Endotoxins break down products of gram-negative pathogens a. They are LPS-related productsb. Acts on immune cells causing secretion of inflammatory cytokines (fever)E. In order to be successful, pathogens usually need to block or avoid the host immune response1. Immune mechanisms that target pathogens that grow extracellularly2. Mechanisms that target pathogens that grow intracellularlyIII. Immune Evasion MechanismsA. Resistance to extracellular immune mechanisms – phagocytosis, complement, and antibodies1. Physical barriers, specific inhibitors, hidingB. Physical barriers: capsule and biofilms inhibit (are resistant to) phagocytosis and compliment binding1. Specific inhibitors of immunitya. Complement inhibitionb. Antibodiy blocking: S. aureus makes protein A that binds the Fc region of antibodiesc. Why doesn’t protein A binding of antibody enhance phagocytosis – Protein A is competing for back end of binding site2. General strategy for avoiding immune mechanisms: hidinga. Viruses are obligate intracellular pathogens – use host cell machinery and components for reproduction- While inside of cells, viruses avoid host antibodiesC. Bacterial pathogens hiding inside of cells1. Prevent fusion of lysosomes with phagosome2. Escape from phagosome by lysing vesicle and more to cytoplasm3. Survive in phagolysosome by detoxifying