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Flashcards

Bacteria and invasion

Bethany Goh III English 68 cards

Bacteria and invasion

Cards in this deck (68)

  1. 1Name the bacteria causing MeningitisNeisseria meningitidis
  2. 2Name the 3 bacteria causing pneumonia and TBMycoplasma pneumoniae
    Legionella pneumophila
    Pseudomonas aeruginosa
  3. 3Name the 4 bacteria causing dysentry and diarrhoeaShigella spp.
    Salmonela spp.
    Yersinia enterocolitica
    Listeria monocytogenes
  4. 4Name the bacteria causing UTIUropathogene Escherichia coli (UPEC)
  5. 5Define: Invasion - for bacterial pathogensAbility of bacteria to reach a sterile site in the host
  6. 6Define: Invasion - for intracellular bacteriaActive process managed by bacteria to enter into non-phagocytic eukaryotic cells
  7. 7Give 5 advantages of invasion for bacteriaTo avoid competitors
    Avoid immune response
    Cross mucosal barrier
    Multiplication and dispersal in the host
    gain access to nutrients
  8. 8Give 2 disadvantages of invasion for bacteriaHow to enter into non-phagocytic cells
    Must survive defences at new site within the cell, e.g. avoid/survive within the lysosomal or phagosomal environment
  9. 9Outline the invasion system 'triggering' (4)Bacteria inject virulence factors directly into the host cell cytoplasm to active their own uptake by the cell
    Bacteria only weakly adhere to the cell
    Bacteria force the cell to extend to the local protrusions that engulf the bacterium (Rho GTPases)
    T3SS-dependent
  10. 10Outline the cell invasion system 'zippering' (2)Entry mediated by high-affinity binding of a pathogen surface protein with a transmembrane receptor on the host cell
    Tight envelopment of the pathogen by the host cell membrane and uptake of the bacteria
  11. 11Give an example of a bacteria that uses a) the trigger mechanism b) the zipper mechanisma) Salmonella spp
    b) Listeria monocytogenes
  12. 12Salmonella is a systemic life-threatening infection. What are its two denominations?Salmonella enterica derivar Typhi (inducing typhoid fever) and Non-typhoidal salmonella (NTS)
  13. 13How many cases and deaths of typhoid fever are there a year?More than 20 million cases
    More than 200,000 deaths
  14. 14What does non-typhoidal salmonella cause? How many cases of these are there annually and how many deaths?Gastroenteritis and bacteremia
    More than 90 million cases annually
    More than 150,000 deaths annually
  15. 15Via which three ways can Salmonella Typhimurium enter into the host?Via M cells
    Via Epithelial cells
    Via Dendritic cells
  16. 16Outline Salmonella Thyphimurium's entry via M cells (3)Entry and translocation though M cells
    Entry into macrophage - survival/multiplication = macrophage apoptosis and hence inflammation
    Invasion of epithelial cell
  17. 17Outline Salmonella Thyphimurium's entry via a) epithelial cells b) dendritic cells (2)a) Trans-epithelial migration --> survival/multiplication
    b)Luminal capture by DC's --> Entry --> systemic dissemination
  18. 18Draw a diagram outlining the 3 methods via which Salmonella Typhimurium can enter the host (10)Draw a diagram outlining the 3 methods via which Salmonella Typhimurium can enter the host (10)
  19. 19What is the trigger mechanism characterised by? (2)Massive ruffles
    Clustering of F-actin beneath the entering bacteria
  20. 20What two distinct T3SS does Salmonella encode for?SPI-1 and SPI-2
    (salmonella pathogenicity island)
  21. 21What is the function of SPI-1? What does it do and where is it found? (3)Cell invasion
    Stimulation of pro-inflammatory response
    Expressed in the lumen
  22. 22What is the function of SPI-2? What does it do and where is it found? (4)Survival and replication inside cells
    Formation of Salmonella containing vacuole (SCV)
    Prevention of endocytic traffic and phagosome maturation
    Expressed inside host cells
  23. 23List 5 things that SPI-1 mediatesCytoskeletal rearrangements
    Triggering of cell entry
    Apoptosis
    Loss of electrolytes
    Inflammation
  24. 24List 3 things that SPI-2 mediatesSystemic spread
    Proliferation in host organs
    Intracellular proliferation
  25. 25What are small GTP binding proteins/small GTPases?Molecular switches that regulate several cellular processes
  26. 26What do small GTP binding proteins regulate? (4)Growth
    Differentiation
    Cytoskeletal organisation
    Trafficking
  27. 27What catalyses GDP --> GTP reaction with Rho GTPases?GEF: Guanine nucleotide exchange factor
  28. 28What dephosphorylates GTP from Rho-GTPases to make Rho-GDP?GAP: GTPase activating protein
  29. 29What small GTPase mediates: Membrane traffickingRAB
  30. 30What small GTPase mediates: Cytoskeleton dynamicsRho
  31. 31What small GTPase mediates: Cell proliferationRas
  32. 32What small GTPase mediates: Nuclear transportRAN
  33. 33What small GTPase mediates: Vesicles transportSAR1/ARF
  34. 34What are the three main small Rho GTPases?RhoA, Rac, Cdc42
  35. 35What do the three small Rho GTPases regulate?Actin cytoskeleton organisation
  36. 36What does RhoA mediateStress fibres
  37. 37What does Rac1 mediateLamellipodia membrane ruffles
  38. 38What does Cdc42 mediateFilopodia
  39. 39What are SopE and SopE2? What do they do? (3)GEF (guanine nucleotide exchange factor) like molecules
    Bind and activate small GTpases Cdc42 and Rac acting as GEF
    Induce membrane ruffling which promotes cell entry
  40. 40What is SopB? What does it do? (4)Phosphatidylinositol phosphatase
    Acts on host phospholipids at the membrane cell
    Stimulates SH-3 containing GEF for RhoG
    RhoG activation induces actin rearrangements and membrane ruffling
  41. 41What does SipA do?Stabilises the actin filaments by inhibiting their depolymerisation by cellular Actin binding proteins (ABP's)
  42. 42What is Fimbrin?An actin cross-linking protein important in the formation of flipodia
  43. 43What do SipB and SipC form?The translocon/pore for secretion of the other effectors into the host cell
  44. 44What does SipC initiate?Actin nucleation via its CTD and NTD
    CTD nucleates the assembly of actin filaments
    NTD induces bundling of actin filaments
  45. 45What do Salmonella inject following internalisation? What is the effect of this? (5)SptP: a GAP (inhibitor of small GTPases)
    SptP is degraded later than SopE/E2 in infected cells
    SptP inhibits both Rac and Cdc42 activated by SopE
  46. 46Once inside the cell, where does Salmonella replicate?Within the SCV: Salmonella containing vacuole
  47. 47What's the effect of Salmonella in the SCV?Redirects the fate of this compartment away from the normal phagosomal pathway
  48. 48Name two bacterial genes required for survival and replication of SalmonellaSifA
    SseJ
  49. 49Recent studies have shown that in epithelial cells, Salmonella is enclosed in the SCV but is also free in the ______cytoplasm
  50. 50Listeria monocytogenes is a _____ _____ disease but can also be transmitted to the ______ by the motherfood borne
    foetus
  51. 51In which situations is listeria monocytogenes most common?In the immunocompromised, newborns (meningitis) and pregnant women (miscarriages, stillbirth)
  52. 52How do listeria monocytogenes enter the host?Cross mucosal barriers and infect a wide range of cell types including macrophages
  53. 53What are the listeria monocytogenes invasion genes? What do they bind to?Internaline A and B
    Internalin A (InlA): binds to cell surface receptor E-Cadherin
    Internalin B (InlB): binds to cell surface receptor Met
  54. 54What is E-cadherin?Transmembrane protein that belongs to a large family of cell-cell adhesion molecules
  55. 55What is the structure of E-Cadherin and what are they required for?Form a large complex with alpha and beta catenins
    Required for the correct formation of adherents junctions between epithelial cells
  56. 56Via which two ways can Listeria invade enterocytes?Via basolateral domain or cell extrusion area
  57. 57How does internalisation of Listeria occur?Via an interaction between Internalin A (InlA) and E-cadherin and subvert signalisation induced by this protein
    Required for crossing of intestinal and placenta-foetus barriers
  58. 58What is Met?Receptor for hepatocyte growth factor
    A protein tyrosine kinase
  59. 59What does binding of HGF to Met activate?Activates cellular survival and proliferation signal
    Induces cytoskeletal rearrangements
  60. 60How does HGF induce ubiquitination and internalisation?By a cathrin mediated endocytosis mechanism leading to degradation of the receptor
  61. 61The Zipper mechanism is InlB-dependent. Outline the acton of InlB.Binds Met receptor and mimics HGF
    Induces autophosphorylation and ubiquitination of Met and takes advantage of endocytic machinery
  62. 62What do the adaptors of Met lead to?activation of class IA PI3K and Rac1GTPases
  63. 63What is internalisation of Listeria dependent on?Actin and Arp2/3 complex
    involves Cdc42-Rac1 and their effectors N-WASP and WAVE
  64. 64Where are InIA and InlB regionally found?InlA: in the intestinal barrier
    InlA and InlB in the placental barrier
  65. 65Listeria express ActA. What is its function?Acts like WASP proteins: recruits actin and Ena/VASP host cell proteins allowing intracellular motility and intracellular spreading via actin polymerisation
  66. 66Define AutophagyProcess used by eukaryotic cells to recycle old or damaged components in response to cellular damage or stress
  67. 67Define XenophagyThe use of autophagy against the invading pathogen: detect and destroy intracellular free bacteria
  68. 68How does ActA escape autophagy?ActA recruits actin and Ena/VASP host cells protecting/masking the bacteria against autophagic recognition

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III Flashcards on Bacteria and invasion , created by Bethany Goh on 06/05/2018.
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Bethany Goh
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