106 - Gut Microbiota Flashcards

1
Q

Proportion of faeces that is bacteria

A

~30%

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2
Q

Type of organism that makes up the majority of GIT microbiome

A

Anaerobic bacteria

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3
Q

Main phyla of GIT bacteria

A

Bacteroidetes, Firmicutes, Actinobacteria, Proteobactiera (relatively rare, EG: E coli)

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4
Q

Similarity of microbiota between twins

A

Under 50% bacterial species shared

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5
Q
Processes that genes from microbiota are important for 
1
2
3
4
A

1) Metabolism
2) Development
3) Immune system
4) Protection against enteropathogens

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6
Q

How can the microbiome aid in development?

A

Intestinal epithelial cell maturation, angiogenesis, lymphocyte development

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7
Q
Factors influencing GIT microbiota
1
2
3
4
5
A

1) Mode of birth
2) Age
3) Diet
4) Antibiotics
5) Genetics and environment
6) Chronic inflammation

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8
Q

How can mode of birth affect microbiome?

A

Vaginal delivery associated with rapid acquisition of Firmicutes, Bifidobacteria.
C-section associated with delayed microbiome development, reduced diversity

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9
Q

How can age affect GIT microbiome?

A

Diversity increases with age

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10
Q

How can diet affect GIT microbiome?

A

Breast milk, low fat/fibre-rich, high fat/high sugar all can affect microbiome

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11
Q

Effect of animal-based diets on microbiome

A

Increases levels of bile-tolerant bacteria (Bacteroides), decreases levels of bacteria that metabolise dietary plant polysaccharides

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12
Q

Two theories explaining why germ-free mice need higher calorie diet to maintain body weight
1
2 i, ii

A
  1. The microbiota directly supply nutrients from dietary
    substances, (eg vitamin B2, vitamin K, biotin, folate,
    CHO from plant sugars – 10% calories)
  2. The microbiota alter metabolic machinery of host cells by:
    i) inducing changes in host genes involved in CHO and
    lipid metabolism, and
    ii) maintaining enterocyte
    differentiation and function (short chain fatty acids,
    SCFA’s)
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13
Q

How do GIT microbiota have a similar effect between individuals, even if the species distribution varies?

A

Metabolic pathways remain stable between individuals in a healthy population (calculated by examining 16s rRNA ofgut microbiota)

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14
Q

Gut microbiota metabolism of carbohydrates

A

Lactose, cellulose, mucins broken down into SCFA

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15
Q

How can gut microbiota lead to synthesis of mucus?

A

Bacterial degradation of host glycans (mucin, chondroitin, sulphate, etc) elicits synthesis of new glycans by host

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16
Q

How can gut microbiota promote gut wall integrity?

A

Produce short chain fatty acids from undigestible
carbohydrates (eg butyrate) that maintain enterocyte
differentiation

17
Q

How can bacteria contribute to adiposity?
1
2

A

1) Complex carbs metabolised to SCFA (acetate, propionate, butyrate)
2) SCFA inhibit histone deacetylase, and metabolic regulation through binding to GPCR.

18
Q

Where are Peyer’s patches located?

A

Small intestine

19
Q

Where in vili do lymphocytes often sit?

A

Lamina propria, intraepithelial lymphocytes

20
Q

Intraepithelial lymphocytes

A

Gamma/delta T lymphocytes, sit in the gut epithelium

21
Q

Cells within the GIT that release IL-22

A

NK cells (NK-22)

22
Q

Role of IL-22 in the gut

A

Increase antimicrobial defence, epithelial repair, barrier integrity

23
Q

Cell subtype that invariant lymphoid cells resemble

A

Th17

24
Q

What do mucosal associated invariant T cells detect?

A

Not completely understood.

Respond to bacterial antigens (EG: riboflavin) presented on an MHC-I-like molecule (are mostly CD8+)

25
Q

NKT cell receptor

A

CD1d, presenting lipid antigen

26
Q

Ways in which DCs in the GIT can sample antigen

A

1) Directly from gut lumen

2) Indirectly, delivered by goblet cells or M cells

27
Q
Functions of gut DCs
1
2
3
4
A

1) In steady state, induce Treg (TGFb), Th2 (anti-inflammatory environment)
2) In inflammatory conditions, induce Th1, Th17
3) Bias B cell isotype switching to IgA
4) Induce mucosal addressin alpha4beta7 on activated T and B cells and receptors for mucosal chemokines

28
Q

alpha4beta7 ligand

A

MAdCAM1 (only expressed on HEV, epithelial cells of mucosal tissues)