module 3 remember Flashcards
describe the p pili
used by UPEC. assembly occurs in an ordered fashion.
PapA - structural component
PapG - adheres to the host cell
PapC - channel which components get transported through
PapD - chaperone which binds and helps components fold correctly.
describe the type IV pili
used by neisseria.
pili with twitching motility
new PilE subunits are added to allow the pili to grow – this is ATP dependent.
PilC is the tip protein which adheres to the human host cell – typically the CD46 receptor
brings adherent bacteria in close proximity to the cell
describe the invasin protein
used by yersinia. this allows for attachment and then internalisation. yersinia is internalised into a vacuole into M cells of the intestine and are released. the invasin protein allows the bacteria to adhere to macrophages instead of being ingested. causes apoptosis of the macrophage, leading to yersinia release, which can then disseminate to other cells.
describe the intimin protein
used by EPEC. The receptor and adhesin are dervied from the bacterium
EPEC adheres using a typve IV pili. using a type 3 secretion system, it injects bacterial proteins. it injects Tir - which is the intimin receptor. this then allows EPEC to bind to Tir through initmin on its outer membrane. this elicits pedestal formation which mediates tight and adherent binding of EPEC to the cell.
describe listerias mechanism of internalisation
internalisation through interaction with the receptor. lnlA of listeria interacts with E-cadherin on the human cell. E-cadherin is normally for anchoring cells together. When lnlA of listeria binds, this activates RhoGTPases. these activate actin polymerisation. actin polymerisation is directional, where monomers are added to one end and dissociate from another. this actin polymerisation allows for localised changes of the F-actin cytoskeleton. The membrane of the cell extends around the bacteria, thus allowing for the internalisation of listeria
describe salmonellas mechanism of internalisation
this is through injection of proteins into the host cell, resulting in major structural changes of the cell. this requires a type 3 secretion system. salmonella injects bacteria-dervied GEFs and GAPs. GEFs cause GDP to form GTP, which results in actin filament polymerisation. this results in ruffling of the cell membrane and causes microvilli to disappear. this allows for internalisation of salmonella. once the bacterium has been internalised, GAPs cause dissociation, causing GTP to form GDP, stopping atin polymerisation. GEF is degraded. this is for avoiding host cell toxicity. salmonella is now internalised, and can now spread between cells
describe toxoplasmas mechanism of internalisation
this is driven solely by the pathogen. it is a result of changes in the actin skeleton of toxoplasma, causing gliding motility. toxoplasma adheres to the cell, and changes in the toxoplasma actin skeleton can cause toxoplasma to move. microneme proteins are pushed left through the plasma membrane, allowing the movement of the bacterium to the right. this allows it to penetrate the host cell and invade it
describe features of phagocytes
- low pH – it has proton pumps on the membrane which pump protons inside the membrane, thus lowering the pH
*ROS – NADPH oxidase complex converts oxygen to superoxide which is then converted to hydroxyl radicle which oxidises bacterial macromolecules
*CAMPS – these are peptides which insert into the membrane of bacteria, causing lysis
maturation of phagocytes occurs through interactions with endosomal compartments.
describe the survival of salmonella
salmonella has the ability to survive in a phagosome as it can tolerate low pH. it lives in an altered phagosome with a low pH, but it is not as low as a normal phagosome.
salmonella has superoxide dismutase enzyme, which converts superoxide to hydrogen peroxide, and catalase, which converts hydrogen peroxide to water and oxygen. this means that superoxide is not converted to hydroxyl radicle, and the bacterial macromolecules are not oxidised.
salmonella can also resist killing by CAMPs. it has a PhoP/PhoQ and PmrA/PmrB system which sense low pH and other factors of a phagosome, and stimulate gene expression to alter LPS accordingly so that CAMPs cannot bind to LPS.
describe the survival of legionella
this avoids fusion between a phagosome and lysosome, creating a phagolysosome which would normally kill bacteria. it does this through a Dot/Icm type 4 secretion system, and injects bacterial proteins which interfere with cellular trafficking. phagosomes mature by interaction with endosomal compartments, meaning that if this process is stopped, legionella can survive. the phagosome will lack characteristics such as low pH, ROS production and protease presence. legionella will contain membranes derived from the ER.
describe the survival of listeria
this has the ability to escape the vacuole. it interacts with 2 different receptors to get internalised into the phagosome. escape from the vacuole is mediated by LLO (listeriolysin O). this is a pore forming toxin which binds to membranes and undergoes cholesterol dependent oligomerisation, resulting in pore formation. this is activated by low pH, ensuring that this process occurs primarily in phagosomes. this causes the vacuole to lyse, thus allowing for the escape of listeria. once the phagosome is destroyed, listeria can move via a motility process involving actin polymerisation, and move to the periphery of the cell, create and protusion and spread to the adjacent cell. the same process of escaping the vacuole occurs, and listeria continues to spread between cells
explain the replication and spread of listeria
listeria uses glucose 1 phosphate as a carbon source. it has Hpt which is a membrane protein that transports gluoce 1 phosphate which then enters the glycolytic pathway.
listeria spreads through actin dependent motility. it subverts human actin to stimulate movement. the monomers add to one end and dissociate from another
describe surface acting toxin - TSST
this is used by S. aureus. TSST is a superantigen, which binds to MHC-II, and activates T cells even when there is no antigen specific to the pathogen present. this causes extreme T cell proliferation, with a dramatic increase of release of IL-2, leading to septic shock. this affects endothelial cells, causes leakage of vessels, and major organs not recieving enough oxygen. TSST also prevents development of antibody production as it interferes with normal immune function
describe diphtheria toxin
diphtheria binds to the host cell, and the receptor gets internalised. the A/B toxin is internalised into a phagosome, and the low acidic pH causes the A and B domain to dissociate. The B toxin creates a pore in the membrane, and the A domain is released. the A domain causes ADP ribosylation of human EF2. EF2 is involved in protein translation, and ribosylation of this means that it cannot bind to tRNA. this stops the ribosome translocation step of protein translation to not occur.
describe cholera toxin
this is an A/B toxin. it causes ADP ribosylating a host GTPase – Gs alpha. this causes cAMP accumulation in the cell. this blocks Na+ import, creating a hypertonic environment. this means that water will move from the blood into the lumen to compensate for this, resulting in diarrhoea in the patient. Cl- efflux is stimulated through activation of the CFTR channel.
cholera toxin gets into the cell through taking advantage of trafficking mechanisms. it moves through the ER, as this is the only compartment with pores, allowing it to get into the cytoplasm
the cholera toxin is acquired by vibrio cholerae through a bacteriophage. cholera adheres to the cell through the TCP adhesin on its bacterial membrane. the TCP adhesin is also a receptor for a bacteriophage which encodes for the cholera toxin. this means that adhesion of vibrio cholerae to the cell is a requirement for acquisition of the toxin. only TCP+ bacteria have the cholera toxin gene
