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MICB 308 > Invasion > Flashcards

Invasion Flashcards

1
Q

pathogen invasion (3)

A
  • pathogens can enter and survive in host cells
  • allows them to breach host epithelial barrier
  • provides them with protected niche for replication and persistence
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2
Q

pathogen mechanism of invasion (2)

A
  • can actively direct their entry into host cells
  • usually done by a protein called “invasin”
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3
Q

invasins (2)

A
  • activate a receptor
  • leads to a signaling event that enables uptake through cytoskeletal rearrangements
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4
Q

mechanisms of particle update into cells (2)

A
  • zippers
  • triggers
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5
Q

mechanisms of particle update into cells: zippers (3)

A
  • sequential engagement of phagocytic membrane with particle surface
  • pseudopod advances no further than receptor-ligand interaction permits
  • partial engulfment where receptor-ligand interactions are
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6
Q

mechanisms of particle update into cells: triggers (2)

A
  • all-or-nothing effect
  • complete phagocytosis
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7
Q

zipper uptake steps (4)

A
  1. initial contact (adherence)
  2. receptor clustering
  3. phagocytic cup formation involving actin polymerization and membrane extension
  4. closure of phagocytic cup and retraction involving actin depolymerization
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8
Q

Yersinia (2)

A
  • enteric pathogens that infect Peyers Patches in the intestine
  • pathogenesis involves translocation across intestinal barrier via M cells, an easy cells for bacteria to breach
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9
Q

M cells (2)

A
  • epithelial cells that lack mucus on their surface and lack microvilli
  • sample their environment and take up particle nutrients and microbes
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10
Q

Yersinia and Invasion: what mechanism does Yersinia use for invasion

A
  • zipper-mediated invasion
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11
Q

Yersinia and Invasion: how does Yersinia access enterocyte cells

A
  • Yersinia translocated through M cells and enters neighbouring enterocytes via the basolateral membrane
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12
Q

Yersinia and Invasion: what proteins are involved in Yersinia invading enterocyte cells (2)

A
  • invasin protein involved in entering enterocytes
  • binds integrin receptor only expressed on basolateral side of enterocytes
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13
Q

Yersinia and Invasion: when is invasion acheived

A
  • when there are sufficient numbers of receptors bound to the invasin through zipper-medicated uptake
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14
Q

How is Yersinia competing with ECM proteins

A
  • integrin receptors bind ECM proteins and use actin to remain in proper formation
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15
Q

Yersinia and Invasion: invasin and ECM affinity to integrin (2)

A
  • affinity of integrin for invasin is very high
  • affinity for invasin is 100x higher than affinity for ECM proteins
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16
Q

Yersinia and Invasion: what occurs as a result of the sufficient amounts of integrin bound to invasin (3)

A
  • tyrosine phosphorylation
  • involves FAK (kinase), PI3 kinases, GTPases Src and Rac
  • cytoskeletal rearrangements and pseudopod engulfment result
17
Q

Listeria monocytogenes and Invasion: what mechanism of invasion

A
  • zipper-mediated invasion
18
Q

Listeria monocytogenes and Invasion: invasin ligand and receptor in enterocytes (2)

A
  • the invasin is Internalin A (InlA)
  • the receptor is E-cadherin
19
Q

Listeria monocytogenes and Invasion: invasin ligand and receptor in hepatocytes (2)

A
  • the invasin is Internalin B (InlB)
  • the receptor is a protein called “Met”
20
Q

Listeria monocytogenes and Invasion: what does uptake involve

A
  • involves clathrin-mediated endocytosis and cytoskeletal rearrangements
21
Q

trigger uptake mechanisms (3)

A
  • mechanism similar to micropinocytosis
  • macropinosomes
  • surface ruffling
22
Q

trigger uptake: mechanism similar to micropinocytosis

A
  • a form of endocytosis that is accompanies by cell surface ruffling
23
Q

trigger uptake: macropinosomes

A
  • large vesicles that serve as a route for cells to take up macromolecules non-selectively
24
Q

trigger uptake: membrane ruffling (2)

A
  • unguided pseudopodia
  • ruffles fall back onto bacteria and this leads to formation of large endosomes, which eventually become smaller
25
Q

trigger: distinct steps (3)

A
  1. filopode formation: membrane ruffles
  2. lamellipode formation: membrane ruffles filled with actin support through polymerization
  3. formation of phagocytic cup made of actin or through adherence
26
Q

Shigella flexneri (3)

A
  • originates from the colon and is extremely infectious
  • initially invades M cells
  • causes “bloody” diarrhea and inflammation, which is crucial for its pathogenesis
27
Q

Shigella and Invasion (2)

A
  • involves over 30 bacterial proteins that mostly encode T3SS apparatus, while the rest are effectors
  • hijacks normal cell signaling pathways to cause massive cytoskeletal rearrangements
28
Q

Shigella Invasion: trigger step 1 (3)

A
  • bacterial proteins IpaB and IpaC form pore in host cell membrane (T3SS) and serve as ligands for host cell receptors
  • this becomes a portal for effectors to enter the host cell
  • triggering results in local destabilization of microtubules by Shigella protein VirA
29
Q

Shigella invasion: trigger step 2 (3)

A
  • activation of cell signaling occurs via many GTP-binding proteins such as CDC42/Rac
  • leads to lamellipode formation
  • several host proteins are involved in mediating actin polymerization and cytoskeletal rearrangements
30
Q

Shigella invasion: trigger step 3 (2)

A
  • final step is actin depolymerization mediated by Shigella protein IpaA
  • IpaA binds host protein vinculin to induce actin depolymerization, resulting in Shigella uptake
31
Q

zipper vs trigger (2)

A
  • zipper results in localized contact-dependent receptor-medicated particle engulfment
  • trigger results in generalized engulfment event that could include neighbouring particles
32
Q

anti-phagocytosis (2)

A
  • some bacteria actively inhibit their uptake
  • secrete protein YopH through T3SS
33
Q

YopH

A
  • phosphatase that overrides kinase that is activated by invasin
34
Q

can one pathogen exhibit both zipper and trigger mediated invasion

A
  • yes, for instance, salmonella can invade host cell using different routes and mechanisms

MICB 308 (22 decks)

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