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34 Cards in this Set
- Front
- Back
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respiratory burst uses what |
NADPH oxidase complex |
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hydrogen peroxide is broken down by what to form what |
myeloperoxidase to hypochlorous acid- most bacterial oxidant in neutrophils |
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reactive nitrogen internediates might play less of a role in what |
neutrophils but neutrophils produce nitric oxide and peroxynitrite- very toxic |
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activated macrophages cause what |
expression if inos- inducible nitric oxide synthase- NOS2 |
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what are the 2 constituent forms of inos in cells |
NOS1 NOS2 calcium independent and causes oxidation of L-arginine |
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what do TH2 and TH1 cytokine do |
balance is competitively regulated Th2- inhibit NO production Th1-enhance no production |
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what does arginase-1 do |
deplete arginine through a STAT-6 dependent mechanism gets ride of argine |
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what happens in reactive nitrogen species in infection |
2 signals increase production causes expression of INOS |
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what are hydrolytic enzymes Ph |
4.5/5.0 |
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how is ph maintaines |
by a membrane bound ATP pump H+/ATPase |
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name a few phagolysosomal enzymes |
nucleases, proteases, glycosidaeses, lipases, phosphatases |
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wha do phagolysosome enzymes do |
significant contribution to cell killing results in the generation for antigenic peptides for class II MHC loading |
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in neutrophil non oxidative mechanisms, what are enzymes |
polypeptides that distrupt the integrity of the pathogen |
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whats a neutroohil non-oxidative mechanism |
neutrophil elastase- produced as a preproenzyme needs to be cleaved before activated dont need alot of it to be toxic |
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what is a target for neutrophil elastase- |
ompA/ in gram negative bacteria |
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what are the types of cell death caused by neutrophils |
apoptosis, autophagy, pyropoptosis, oncosis and netosis |
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describe apoptosis |
doesn’t produce an inflammatory response requires caspases can recruit phagocytes |
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what is killing by autophagy |
cellular starvation not an inflammatory response |
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explain killing my pyroptosis |
programmed cell death resulting in cell lysis inflammatory response |
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explain killing my oncosis |
cell death lysis inflammatory response and tissue damage |
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explain netosis |
using oxidative stress- can cause damages chuck out proteins and histone from cell and produce a net so it bacteria get stuck they are immobilised so other neutrophils and macrophagess can destroy it |
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describe 2 signals by apoptosis |
intrinsic signal (high ROS) extrinsic ( tnf alpha, fas with fasl or trail |
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what happens in apoptosis with low conc tnf |
delays apoptosis high conc increases incidence |
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how can apoptosis be delayed |
if infection is present- exposure to inflammatory mediators from bacteria |
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how does co operation in killing occur |
transferred molecules increase ability to kill ingest apoptotic neutrophils- obtain granules with increase ability to kill mycobacteria |
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explain how cells need intracellular iron |
need iron to grow extracellular iron is loaded onto transferrin recetor CD71 on cell membrane iron is internalised during phagocytosis co receptor in generation of ROI too much iron cell can become infected |
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how to stop a pathogenic cell from growing using iron |
CD71 is down-regulated so cell takes up less iron and stops it from growing |
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where are defensins present |
neutrophil granulocytes |
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what are defensins |
small cystein rich cationic proteins |
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what do defensins do |
bind to microbial membrane an once embedded form pore like membrane defects |
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what amino acids do defensins have |
29-35 amino acids with 6 invarient cysteine residues produced as a precursor |
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what do defensins inhibit |
protein kinase C |
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why arent phagocytes damaged by ros |
mitochondria have a very active cytochrome oxidase- decrease oxygen availability cytochrome c- catalyses oxidation of superoxide ion to oxygen- protective presence of superoxide dimutase- converts superoxide to hydrogen peroxide which escapes mitochondrion because its more permeable to it |
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what happens if there is very high ros concentrations |
release of cytochrome c into cytosol catalyses oxidation of superoxide ion into oxygen oxidation of cytochrome B5 on outter mitochondial membrane upsets electron transport chain prevents oxygen being converted into superoxide ion inhibition of krebs |
