Lecture 10 - Bacterial Invasion Flashcards

1
Q

Why might bacteria invade?
1)
2)
3)

A

1) Obligate intracellular parasite
2) Avoid immune system
3) Penetrate to deeper tissues

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2
Q

Two mechanisms of invasion

A

1) Zipper

2) Trigger (ruffling)

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3
Q

Host cell function exploited by zipper

A

Receptor-mediated endocytosis.

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4
Q

Host cell function exploited by trigger

A

Macropinocytosis

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5
Q

Which invasion mechanism does Listeria use?

A

Zipper

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6
Q

Basic principle of zipper
1)
2)
3)

A

1) High-affinity binding to host cell
2) Induces receptor immobilisation and crosslinking
3) Results in receptor-mediated endocytosis

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7
Q

Basic principle of trigger
1)
2)
3)

A

1) Resembles cell ruffling caused by hormones or hormones
2) Bacteria induces large-scale actin polymerisation, ruffles on host cell membrane
3) Macropinocytosis

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8
Q

Is Listeria monocytogenes Gram + or -?

A

Gram +

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9
Q

How does Listeria normally enter the body?

A

Food-borne

Soft cheeses

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10
Q

Why can Listeria be very dangerous?

A

Can cross maternoplacental barrier, blood-brain barrier

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11
Q
How does Listeria enter host cells?
1)
2)
3)
4)
5)
A

1) Zipper
2) Bacterial surface covered with internalin protein
3) Internalin binds to E-cadherin
4) E-cadherin binds to internalin all over bacterial surface, causing host-cell membrane to envelop bacterium (receptor clustering)
5) Bacterium is internalised

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12
Q

Proof of internalin effectiveness

A

Beads coated with internalin can invade cells

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13
Q

Another term for internalin

A

InIA

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14
Q

E-cadherin function

A

In tight junctions

Connects actin to structures external to cell

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15
Q

Is zipper or trigger more complex?

A

Trigger
Trigger uses far more proteins (~50) than zipper (as few as one)
Zipper is a passive process. Trigger is an active process

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16
Q

Bacterium that uses zipper

A

Listeria monocytogenes

17
Q

Bacteria that use trigger

A

Shigella flexneri

Salmonella enterica

18
Q

Is Shigella Gram + or-?

A

Gram -

19
Q

Shigella spread

A

Person-person

Water-borne

20
Q

Effects of Shigella infection

A

Bacillary dysentery

Bloody diarrhoea

21
Q

How does Shigella differ from other E. coli?
1)
2)

A

1) Acquired virulence plasmid, pathogenicity islands

2) No flagella or fimbriae, to reduce inflammatory response from bacterial proliferation

22
Q

Protein making up Shigella T3SS shaft

A

MxiH

23
Q

What does MxiH do?

A

Makes up shaft of Shigella T3SS

24
Q

Functions of ipaB, ipaC, ipaD

A

Inserted into host cell by Shigella, induce membrane ruffling (particularly ipaC)

25
Q

Shigella proteins that induce membrane ruffling

A

ipaB, ipaC, ipaD

ipaC most important

26
Q

Which cells does Shigella invade?

A

M cells

27
Q

Host cell proteins activated by Shigella to polymerise actin

A

RhoGTPases

28
Q

Does Salmonella use zipper or trigger?

A

Trigger

28
Q

Host cell proteins targeted by Shigella

A

Actin, vinculin, tubulin (cytoskeletal proteins)

28
Q

Proteins used by Salmonella to invade

A

Sip proteins, encoded on SPI-1

28
Q

Proteins encoded by SPI-1

A
Sip proteins (for Salmonella)
T3SS
28
Q

Targets of Sip proteins

A

Host cell cytoskeleton, GTPases

28
Q

Number of T3SS’s possessed by Salmonella

A

Two

28
Q

What are the different Salmonella T3SS functions?

A

T3SS 1 - Induce host cell membrane ruffling

T3SS 2 - Escape from endosome, secrete Ssa

28
Q

Ssa proteins

A

Effector proteins secreted by Salmonella T3SS number 2

28
Q
SPI-1 effects
1)
2)
3)
4)
A

1) Invasion
2) Cytoskeletal rearrangements
3) Inflammation
4) Diarrhoea

28
Q

SPI-2 effects
1)
2)
3)

A

1) Avoid intracellular antimicrobial defences
2) Modification of vacuole trafficking
3) Intracellular replication and survival

28
Q

Broadly different roles of SPI-1 and SPI-2

A

SPI-1 - Invasion

SPI -2 - Intracellular survival