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Microbiota On Mucosal > C7- Fungal Collaborators And Competitors > Flashcards

C7- Fungal Collaborators And Competitors Flashcards

1
Q

What is ammensalism

A

Where one has negative effect on the other with no gain unlike parasitism

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2
Q

What sorts of things can bacteria modulate of fungi

A

Antifungal susceptibility, capsule formation, growth, biofilm, hyphal development

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3
Q

What sorts of things can fungi modulate on bacteria

A

Growth, antibiotics, virulence traits like iron acquisition, quorum sensing and biofilm

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4
Q

Candida albicans and pseudomonas aeruginosa - example 1

A
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5
Q

What is pa found in

A

Cystic fibrosis lung

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6
Q

What do it do to hyphae directly

A

Binds hyphae in response to quorum molecule homoserine lactose and kills them

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7
Q

What phenazines can pa release

A

Pyocyanin and pyorubin

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8
Q

What are these important according to major study on morphology effects and how do these phenazines do this

A

Block biofilm formation and hyphal formation

By repressing respiration in candida

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9
Q

Why does phenazine increasing o2 levels in biofilm important (found during experiments)

A

Because they’re usually anaerobic to allow colonies of anaerobes to develop

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10
Q

How did they find it was stopping respiration

A

Dye TTC which turns red by reduction by the ETC didnt happen

Lack of red in presence with phenazines

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11
Q

How does conversely, pa induce fluconazole resistance of candida

A

Homoserine lactose induces efflux pump expression

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12
Q

Which structure is similar to homoserine lactone which indicates its mechanism of action on hyphae (also blocks hyphal growth)

A

Farnesol

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13
Q

Which gene do pa have for iron acquisition which is compromised by fungi

A

Pyochelin genes

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14
Q

Which lung fungi can block growth and biofilm formation of pa important for virulence in Cystic fibrosis

A

Af through its gliotoxin

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15
Q

Example 2 - lactobacillus app and c. Albicans

A
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16
Q

What product of gut lactobacillus masks b glucan (immune escape) and can be used as a c source for growth of ca

A

Lactate

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17
Q

How does it remodel the cell wall

A

Through Gpr1 sensor of lactate and signal transduction to remodel b glucan

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18
Q

Which lactobacillus has chitinase activity which blocks yeast to hyphal formation which is good for us in contrast

A

Rhamnosis GG

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19
Q

In mouse model, what does scfa (also produced by commensals like lactobacillus) like butyrate help to stop overgrowth which is stopped in antiobiotic treatment (potentially important in Ibd)

A

Filamentation and biofilm formation

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20
Q

T6ss and microbial competition

A
21
Q

Explain the structure of a t6ss

A

You have a sheath which contracts during firing event
Then base plate
Then a membrane complex/HCP tube which pushes effector through the vgrg and paar(needle end)

HCP-vgrg-paar structure pushes effectors into target cell

22
Q

What depolymerises the sheath to decontract it after a firing event, allowing it to reset for new firing event

A

TssH

23
Q

What do resistant bacteria have which neutralises effector proteins

A

Immunity proteins which bind

24
Q

Give a few examples of t6ss use

A

Inter bacterial competition
Nutrient scavenging
Killing of fungi
Host cell invasion/killing

25
Q

Which bacteroides can control other popn of bacteroides like b theta or ovatus which don’t have it through t6ss

A

Fragilis

26
Q

What is resistant to this killing

A

Proteo bacteria like ecoli

27
Q

Give example of a bacteria which uses its t6ss to kill fungi in inter kingdom competition

A

Serratia marcescens

28
Q

Incubation of sm with the sach cerevisiae, c glabrata and c albicans does what compared to t6ss mutants

A

Kills them

29
Q

Which effector previously invoked in bacterial bacterial competition was later found to only affect c albicans killing not the other 2

A

Tfe1

30
Q

How did they later identify again tfe 1 and other like tfe2

A

They did a ko of tsse component of the base plate so that effectors would accumulate in fungi

Then did quantitative proteomics on wt vs tsse mutant should see toxin accumulation

and found tfe1 and tfe2 hits and proteins like hcp which validated the t6ss model

31
Q

What does ko of tfe2 effector do unlike tfe1 ko

A

Partially Rescues ca, cg and sc not just ca

32
Q

What does ko of both effectors show unlike if only 1 is ko causing partial rescue

A

Same phenotype as having a t6ss ko (large survival)

33
Q

Doing cryo-tem of sm with yeast Candida/sach cells shows what

A

Necrotic cells/ lysed in presence of t6ss but not in tsse mutant and in contact

Ko of tfe1 showed rescue aswel of necrosis/lysis of Candida albicans

Loss of granules in tfe2 mutant when incubated with glabrata and sach cer

34
Q

When you express a plasmid into the fungi with tfe1 or 2 into s. Cerevisae what happened. Was tfe2 found to kill the cells or jus cause growth arrest of s.cer specifically (which stopped when stopped tfe2 expression)?

A

Tfe1 had no toxicity effect at low levels but tfe2 always toxic

Found in liquid culture that once you stop tfe2 exp in cerevisiae then growth is rescued so it isn’t killing them.

35
Q

How did studies on sach cer find the mechanism tfe1 uses is membrane transport interruption/ membrane depolarisation

A

Dibac4 staining which stains cells which aren’t respiring/no etc/membrane depolarisation (opposite of ttc)
Showed staining of sach cer expression of tfe1

36
Q

Are hyphal tup1 ko candida also killed by sm or just yeast

A

Both

37
Q

How is tfe1 as a membrane depolarising toxin also supported by quantitative proteomics when candida incubated with the diff effectors wt/mutant

A

No target proteins which are upreg or downregulated in its presence (no diff in mutants vs wt)

So suggests it targets membrane not specific proteins

38
Q

How many proteins are differentially upreg or downregulated in tfe2 presence

A

30

39
Q

What are downregulated vs upregulated

A

Sulfate assimilation parhway downregulated (way sulfur is acquired for growth)

Upreg of arginine synthesis

40
Q

What does this indicate

A

Imbalance of nutrients/ depletion of nutrients leading to starvation, autophagy and death

41
Q

Other fungi- bacteria interactions

A
42
Q

Which bacteria in oral mucosa constantly found in biofilm with Candida albicans to form plaques or caries/tooth decay

A

Strep mutans

43
Q

How is it suggested this biofilm forms

A

Through farnesol signalling of candida which induces glucosyltransferases by mutans to increase ecm component of biofilms

44
Q

Which 2 bacterial commensals found in mouse models sufficient in stoping candida overgrowth/colonisation (eg in Ibd) - FAN 2015

A

Blautia producta (firmicute) and b theta

45
Q

How in mice models after 2 weeks was ca undetected. The same molecule also reduced invasive disease death by 50% in mouse model

A

Through inducing ll37 whcih is anti-candida by hif1a tf induction

46
Q

Does proteobactedia have the same effect through ll37

A

No- showing importance of immunomodulatory firmicute and bacteroidetes with other examples like b fragilis and clostridia/f. Prausnitzii

47
Q

Why is hoarau 2016 been controversial

A

Because s. Marcescens shown to have a t6ss which would suggest it is not mutualistic with candida

48
Q

Why are gpi anchored mannoproteins with n-mannan being on the outer cell wall very important

A

To hide b glucans which are very immunogenic

49
Q

Which author / research study first coined the idea that l Reuteri in mouse models are critical for trp metabolism induced ilc3 which release il22- which they found to have antagonistic effects on c albicans (example of a ammensalistic relationship)

A

Zelante 2013

Microbiota On Mucosal (22 decks)

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