L8 - Microbiota And Pathogens Flashcards

(51 cards)

1
Q

Which microbiota via metagenomics of patients found to provide resistance to vibrio cholera

A

Ruminococcus obeum

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2
Q

How

A

Using autoinducer 2 as a quorum sensor which reduces colonisation factors of vibrio

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3
Q

What do bacteria regulste during quorum sensing

A

Gene expression

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4
Q

What does population desnity habe to do with quorum signalling

A

Rleease of molecules like AI can increase to a certain conc when larger popn of bscteria. This readhes a threshold where they can turn on gene regulatory pathways eg to cause virulence

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5
Q

AI1 is used by microbiota to try tsckle ehec. How does ehec avoid it

A

Senses ai1 via sdiA receptor and modulates it gene exp so it can survive in a new niche

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6
Q

What article talks more about quorum snesing

A

Miller 2001

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7
Q

What pathways of genes turned on due to wuorum snesing (miller 2001)

A

Motility, virulence, biofilm production, symbiosis

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8
Q

Which types of bacteria use AI1 (miller 2001)

A

Gram +ve

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9
Q

Whst do gram negstice use in quorum sensing as a moleculr (miller 2001)

A

Oligo peptides

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10
Q

What type of secretort ststem does cholera have

A

T6ss

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11
Q

What does t6ss do

A

Physicallt attack and kill commensals of cholera

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12
Q

Which microbiota help reduce t6ss expression by cholera causing increase in commensals

A

Bifido bifidum

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13
Q

How

A

Modify bilr acids into deoxycholic acid which downregulates t6ss

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14
Q

How do microbiota actuvate nadr from the enteric nervous system

A

Deconjugate it from glucoronic acid by glucoronidase

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15
Q

Which pathogens use nadr snesing to turn on virulence genes suppsoedly

A

Salmonella and ehec

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16
Q

What sneses nadr in ehec particularly

A

Qsec histidine kinase

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17
Q

What does qsec histidine kinase do with ehec

A

Increase exp of t3ss via Locus of enterocyte wffacement activation rcoding t3ss. Also other cirulence genes eg for shiga toxin

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18
Q

What tpyes of a pathogen is salmonella

A

Facultstive ic parhogen (xan be both aerobic and anaerobic)

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19
Q

What types of salmonella are there

A

Enterica from food

Typhi causinf typhoid fever

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20
Q

How is typhi systemic

A

Allow escape via the mesentric lymph nodes

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21
Q

Where do modt salmonella die

A

Stomach (unless turn on acid response systems)

22
Q

What expresses t3ss in salmonella

A

Spi1 and spi 2

23
Q

What is injected into epi crlls from t3ss which allows invagination of crll

A

Effector rpoteins which rearrange cytoskeleton

24
Q

What are aalmonella contained in within crlls

A

Salmonella containing vacuoles

25
What does pi 19 encode
T6ss in s. Gallinerum (bird fever) and cholera
26
What apecialised epi fells do salmonella prefer to enter cia t3ss
M cells
27
Whats the difference between sp1 and sp2 t3ss
Spi1 allows entry into epi cells Spi2 allows survival in epi / macrophages within the scv
28
What does nutrient availability depend on
Diet Microbiota composition
29
How dors inflammation cause dysbiosis
Refuced obligate anaerobes ie commesals Increase in facultative anaerobes pathognes like ehec or salmoenlla
30
Which cytokine is released in inflammation allowing fucose release ftom mucus carbs
Il 22
31
What types of bscteria can utliise fucose as a nutrient
Ecoli
32
What bacteria is a model for ehec and epec
Citrobacter rodentium
33
Other than nutrients, what else does inflammation increase
Alternative electron acceptors in non anaerobic
34
Which gene is activattd during inflammation with ifn y and other cytokines
Duox2- hydrogen peroxide production (a ROS)
35
What thpes of diseases have increased duox2 from epi cells
Uc
36
Ehat enzyme is upregulsted by nos2 due ti inflammatory cytokines
No synthetase
37
How is no from nos involved in nitrate resp bu pathogens
Exposed to free radicals to produce peroxynitrate which can be concerted to nitrates
38
How do ros and rns (no derived) speciies form nitrates in inflammation
They react together ans then allow nitrate resp from nitrate generation = growth of enterobacteria
39
What does nitrate resp drive growth of as an alternative nutrient
Commensal and apthogenic ecoli aswell as salmonella. (NOT ANAEROBIC COMMENSALS)
40
What are the 2 rypes of alternative electron acceptors in parhogens and commensal ecoli
Tetrathionate and nitrate
41
Why is inflammation infuced by things like salmonella and ehec
Allows production of the AEA for alrernate food sources for growth
42
How do pstjogens stimulate inflammation
Prr causing inflammatory cytokine release
43
Which 3 things do the il22 and ifny etc increase
Lipocalin 2, ros and nos (aso fucose from il22)
44
What does lipocalin 2 do to stop commensal eg commensal ecoli
Blocks fe acquisition which means they stop growing
45
Which inflammatory cells increase ros production
Neutrophils
46
What do ros from neutrophils do
Convert thiosulphate to tetrathionate which is used as an AEA for thiosulphatw resp eg salmonella
47
What do microbiota release which is converted to thiosulfate allowing tetrathionate profuction
Hydrogen sulphate
48
What nutrient is ysed as for carvon source by salmonella from epi cells
Ethanolamine due to its new AEA it allows salmoenlla to yse ethanolamine
49
Why does ethanolsmine caused dysbiosis aswell as the nitrate/ tetrathionste AEA
Becaude microbiota cannot use them as a carbon source
50
Which srticle talks about effector proteins from t3ss
Srikanth et al 2011
51
Which protein in t3ss is responsible for inducing inflammation and also actin polymerisation + bundling for invaginstion
SipA