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Molecular Microbiology > Lecture 8: Host-pathogen interactions > Flashcards

Lecture 8: Host-pathogen interactions Flashcards

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1
Q

For which diseases do Kochs postulates not hold true?

A

• Presence of agent in healthy animals.:
(asymptomatic carrier may cause disease incidentally; Neisseria meningitidis, Haemophilus influenzae, Streptococcus pneumoniae)
• No animal model available
• Bacteria non culturable
• The infection might be a secondary effect
• E.g. a genetic condition (for example cystic fibrosis)
• Bacteria might co-colonize with the actual infective agent

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2
Q

Infection vs colonization?

A

Colonization = lives in harmony on the body. Infection = invades the body.

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3
Q

What is a virulence factor?

A

Any (gene) product that is involved in the survival and persistence in the host.

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4
Q

A molecular Koch’s Postulate ?

A

 A virulence/pathogenicity Factor should be present in all disease-causing variants of a bacterial species
 Knocking-out of the gene should result in reduced virulence/pathogenicity of bacterium
 Reintroduction of the gene should lead to restoration of virulence

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5
Q

Virulence factors are involved in?

A
  • Adhesion
  • Tissue damage
  • Defence (immune system)
  • Regulation
  • Metabolism
  • Spreading
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6
Q

Which type of secretion system is used for adherance?

A

T3SS. Secretes effector proteins directly from bacterial cytoplasm into host cell

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7
Q

T3SS is evolutionary linked with?

A

Flagella

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8
Q

How does EHEC adhesion go? (E.coli adhesion to epithelial cells: virulence factor. depletion of microvili, makes pedestals)

A 
Bacterial adhesin: Intimin
Receptor on cell surface: Tir
• Translocated Intimin Receptor
• Inserted in host membrane via Type 3 secretion system, binds to intimin in bacterial membrane
Tir receptor is phosphorylated (signal transduction): recruits NPF
• Recruits cytoskeleton proteins
• Nucleation of actin fibers
• Makes pedestals
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9
Q

NPF: what does it do?

A

Nucleation promoting factor: initiates actin polymerization.

Activated by small GTPases (Rac/CDC42) or tir

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10
Q

Pili can also be virulence factors. Targets on cell surface can be?

A
  • Glycolipids
  • Sugar molecules
  • Proteins (extra-cellular matrix, surface proteins)
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11
Q

UPEC adhesion = one of most well known pili interactions. What happens and what is possible treatment?

A

UPEC adhesion.
Tip protein binds to bladder wall:
binds to mannos of glycoselated proteins.

Treatment: take lot of mannose: competing compound, bacteria cannot adhere anymore.

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12
Q

Non-fimbrial adhesins: name 2?

A

• Autotransporters
• Outer Membrane Proteins
> Close to cell surface

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13
Q

Advantages Living inside host cells?

A

Shielded from humoral antibodies

-Less competing bacteria for the same resources

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14
Q

Disadvantages?

A
  • Lysosomal degradation
  • Autophagy
  • Alarming the immune system
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15
Q

Two main types of entry mechanisms?

A
  1. Trigger mechanism (massive cytoskeletal changes). Direct interaction with cytoskeleton by injecting effectors through secretory system (T3SS or T4SS)
  2. Zipper mechanism (modest cytoskeletal changes). Started by interaction between bacterial protein and eukaryotic receptor (indirect activation of cytoskeleton)
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16
Q

Trigger-mediated invasion: - Via T3SS. Bacterial effectors trigger signal transduction route. What does effector SopE do?

A

> Sop E leads to changes in cytoskeleton & vesicle-mediated uptake.

17
Q

SopE needs to activate NPF. How is NPF activated?

A

NPF: needs to get activated to have actin polymerization by CDC42, Rac or Rho (small GTPases)
-> upon activation of GTPases in GTP-bound state they activate the NPF

GAP: turns off
GEF: turns on (GDP-> GTP)

So, GEF is needed.

18
Q

SopE is a GEF protein.. What does it do?

A

Entry into cells via actin polymerization regulated by the GEF SopE. It removes the GDP and replaces it with a GTP. This activates Rec -> NPF active -> actin polymerization.

19
Q

Overview

A

• Trigger-mediated invasion is via type 3 or 4 secretion systems
• Direct activation of cytoskeleton via secreted effectors
- Actin fibers
- Signal transduction
• Example:
- Salmonella, SopE
Activates CDC42/Rac  NPF  actin polymerization

20
Q

How can listeria come in via the zipper mechanism?

A

Binding E-cadherin triggers endogenous host-signaling (rho gtpases -> NGF) -> re-arrangement of the cytoskeleton

21
Q

Listeria getting inside: 2 pathways via zipper-mediated invasion

A

• Via cell surface receptors
Involved in receptor-mediated endocytosis/vesicle formation
• Activation of cytoskeleton rearrangements
-Actin fibers
-Signal Transduction
• Examples:
Internalin A (InlA) of ListeriaBinds E-cadherin
Internalin B (InlB) of ListeriaBinds Met-receptor

22
Q

Escape from the endosome: molecules ensure the phagosomal membrane is dissolved. Bacteria ends up in cytosol. Needs to replicate and move around. Also expresses a protein (ActA) What does it do?

A

ActA functions as an NPF (doesn’t recruit it). Causes direct actin polymerization and propulsion of the bacteria into neighbouring cells
-> ActA displays structural and functional mimicry of NPF

23
Q

What are two ways to escape from immune reaction?

A
  • Inhibit immune responses

* Mimicry of host components (structures on surface)

24
Q

What is the red queen hypothesis in terms of coevolution?

A

Red Queen hypothesis: Same for coevolution of the immune system. Evolutionary change (novelty) gives a temporary advantage, but after adaptation of the pathogen he end result is similar.

25
Q

Bacterial response to iron withdrawal?

A
  • Direct uptake of binding to host molecules

- Production of siderophores (molecules secreted by bacteria that have very high affinity for iron.

25
Q

Bacterial response to iron withdrawal?

A
  • Direct uptake of binding to host molecules

- Production of siderophores (molecules secreted by bacteria that have very high affinity for iron.

25
Q

Bacterial response to iron withdrawal?

A
  • Direct uptake of binding to host molecules

- Production of siderophores (molecules secreted by bacteria that have very high affinity for iron.

26
Q

What is one of the strongest siderophores with an incredible high affinity?

A

enterobactin

27
Q

-> Some pathogenic E.coli strains produce a second siderophore: aerobactin which binds iron less well than enterobactin. Why make 2?

A

Host captures away enterobactin to keep it from reaching the bacteria. Bacteria then makes aerobactin which is not being captured.

Molecular Microbiology (12 decks)

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