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Mucosal Surfaces > L8 - Microbiota And Pathogens > Flashcards

L8 - Microbiota And Pathogens Flashcards

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
Q

What does pi 19 encode

A

T6ss in s. Gallinerum (bird fever) and cholera

26
Q

What apecialised epi fells do salmonella prefer to enter cia t3ss

A

M cells

27
Q

Whats the difference between sp1 and sp2 t3ss

A

Spi1 allows entry into epi cells

Spi2 allows survival in epi / macrophages within the scv

28
Q

What does nutrient availability depend on

A

Diet

Microbiota composition

29
Q

How dors inflammation cause dysbiosis

A

Refuced obligate anaerobes ie commesals

Increase in facultative anaerobes pathognes like ehec or salmoenlla

30
Q

Which cytokine is released in inflammation allowing fucose release ftom mucus carbs

A

Il 22

31
Q

What types of bscteria can utliise fucose as a nutrient

A

Ecoli

32
Q

What bacteria is a model for ehec and epec

A

Citrobacter rodentium

33
Q

Other than nutrients, what else does inflammation increase

A

Alternative electron acceptors in non anaerobic

34
Q

Which gene is activattd during inflammation with ifn y and other cytokines

A

Duox2- hydrogen peroxide production (a ROS)

35
Q

What thpes of diseases have increased duox2 from epi cells

A

Uc

36
Q

Ehat enzyme is upregulsted by nos2 due ti inflammatory cytokines

A

No synthetase

37
Q

How is no from nos involved in nitrate resp bu pathogens

A

Exposed to free radicals to produce peroxynitrate which can be concerted to nitrates

38
Q

How do ros and rns (no derived) speciies form nitrates in inflammation

A

They react together ans then allow nitrate resp from nitrate generation = growth of enterobacteria

39
Q

What does nitrate resp drive growth of as an alternative nutrient

A

Commensal and apthogenic ecoli aswell as salmonella. (NOT ANAEROBIC COMMENSALS)

40
Q

What are the 2 rypes of alternative electron acceptors in parhogens and commensal ecoli

A

Tetrathionate and nitrate

41
Q

Why is inflammation infuced by things like salmonella and ehec

A

Allows production of the AEA for alrernate food sources for growth

42
Q

How do pstjogens stimulate inflammation

A

Prr causing inflammatory cytokine release

43
Q

Which 3 things do the il22 and ifny etc increase

A

Lipocalin 2, ros and nos (aso fucose from il22)

44
Q

What does lipocalin 2 do to stop commensal eg commensal ecoli

A

Blocks fe acquisition which means they stop growing

45
Q

Which inflammatory cells increase ros production

A

Neutrophils

46
Q

What do ros from neutrophils do

A

Convert thiosulphate to tetrathionate which is used as an AEA for thiosulphatw resp eg salmonella

47
Q

What do microbiota release which is converted to thiosulfate allowing tetrathionate profuction

A

Hydrogen sulphate

48
Q

What nutrient is ysed as for carvon source by salmonella from epi cells

A

Ethanolamine due to its new AEA it allows salmoenlla to yse ethanolamine

49
Q

Why does ethanolsmine caused dysbiosis aswell as the nitrate/ tetrathionste AEA

A

Becaude microbiota cannot use them as a carbon source

50
Q

Which srticle talks about effector proteins from t3ss

A

Srikanth et al 2011

51
Q

Which protein in t3ss is responsible for inducing inflammation and also actin polymerisation + bundling for invaginstion

A

SipA

Mucosal Surfaces (33 decks)

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