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Z MD1 GI block > Microbiota > Flashcards

Microbiota Flashcards

0
Q

predominant phyla of the gut

A

Bacteroidetes and Firmicutes
then Actinobacteria
Proteobacteria relatively rare

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1
Q

predominance of gram positive and gram negative bacteria in different places of the body

A

throat, skin and vagina - predominantly gram positive

gut - predominantly gram negative

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2
Q

are the gut bacteria predominantly anaerobic or aerobic

A

anaerobic - 99.9%

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3
Q

what proportion of bacteria of the microbiota are shared between twins

A

<50%

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4
Q

the genes provided by the microbiota contribute to what

A
  • metabolism (carbohydrates, vitamin metabolism/biosynthesis, energy, drugs)
  • development
  • the immune system
  • protection against enteropathogens
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5
Q

what 6 factors can influence the gut bacteria

A
  • mode of delivery
  • age
  • diet
  • antibiotics
  • genetics and environment
  • chronic inflammation
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6
Q

how does the mode of birth delivery influence the microbiota

A
  • vaginal delivery is associated with rapid acquisition of Firmicutes and Bifidobacteria
  • caesarian birth is associated with delayed microbiota development with restricted diversity, and start off with a higher than normal proportion of Protobacteria
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7
Q

what changes in the microbiota are seen over the first few months of life

A
  • initially - microbiota are relatively limited with predominantly Firmicutes and a little bit of proteobacteria involved in lactose breakdown
  • 2-3 months - bacteria changes to get used to breaking down plant based food
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8
Q

what types of diets can influence the microbiota

A
  • high fat/low fibre
  • low fat/high fibre
  • animal based
  • plant based
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9
Q

how does animal based diets alter the microbiota

A

decreases the levels of bacteria that metabolise dietary plant polysaccharides and increase levels of bile-tolerant bacteria (Bacteroides)

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10
Q

Which phyla of bacteria are bile resistant

A

Bacteroides

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11
Q

which antibiotic has long term effects on the gut microbiota?

A

vancomycin - gut microbiota dont go back to original

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12
Q

2 mechanisms for gut microbiota playing a role in nutrition

A
  • directly supply nutrients from dietary substances (as we dont have the genes to metabolise these substrates)
  • alter metabolic machinery of host cells
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13
Q

which dietary substances do the microbiota directly supply us

A

vitamin B2, vitamin K, biotin, folate

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14
Q

how do microbiota alter metabolic machinery of host cells

A
  • induce changes in host genes involved in carbohydrate and lipid metabolism –> contribute to adiposity
  • maintain enterocyte differentiation and function by producing SCFA from undigestible carbohydrates
  • induce changes in host genes affecting angiogensis by producing SCFA
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15
Q

what do the microbiota do to carbohydrates

A

break down lactose, cellulose, mucins –> short chain fatty acids

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16
Q

how do the microbiota affect bile acids

A

dehydroxylation of cholic acid in the gut –> metabolises this to desoycholic acid - allows resorption back into the liver via the enterohepatic circulation

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17
Q

which amino acids do microbiota especially metabolise for us

A

lysine and threonine

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18
Q

what is MALT

A

mucosa-associated lymphoid tissue

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19
Q

what are the lymphoid tissue in the gut

A
  • isolated lymphoid follicles in the large and small intestine
  • Peyers patches in the small intestine - ileum
  • Intraepithelial lymphocytes in the LP
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20
Q

what is the role for ILFs and Peyers patches in the gut

A

sites for induction of T and B cell activation

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21
Q

innate defences of the gut in general

A
  • peristalsis
  • acid
  • mucous layer/glycocalyx
  • enterocytes
  • innate lymphocytes
  • mechanisms for “controlled” antigen access
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22
Q

explain the mucous layer of the gut

A

associated with the enterocytes - act as a molecular sieve, so the commensals held at “arms length”

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23
Q

How do enterocytes contribute to innate defences

A
  • barrier - tight epithelial junctions
  • regular replacement of enterocytes
  • secrete immunomodulatory cytokines and chemokines
  • paneth cells secrete antimicrobial factors
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24
Q

how do goblet cells contribute to innate defenses

A

secrete mucins, lysozyme and lactoferrin - inhibiting the growth of micro-organisms

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25
Q

what are the innate lymphoid cells of the gut

A

lymphoid tissue inducer cells
intraepithelial lymphocytes (IELs)
NK cells

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26
Q

what do lymphoid tissue inducer cells do

A

stimulate recruitment of DCs, T and B cells to peyers patches and ILFs

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27
Q

Role of IL22 in innate gut immunity

A

enhances antimicrobial defence and epithelial repair and barrier integrity

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28
Q

what is special about the macrophages of the gut

A

they are HYPOresponsive to TLR signalling - hard to stimulate them

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29
Q

where are M cells located

A

directly over the sites of organised lymphoid aggregates

30
Q

structure of M cells

A

possess a folded luminal surface (no villi)
lack a thick glycocalyx
dont secrete mucus
(microbial access easier)

31
Q

function of M cells

A

deliver antigens directly to the cells in organised lymphoid aggregates

32
Q

function of DCs in the gut

A

sample antigen from the intestinal mucosa and induce a variety of T cell differentiation pathways

33
Q

how do DCs sample antigen from the intestinal mucosa

A
  • directly (put there processes through the tight junctions between enterocytes –> lumen)
  • indirectly (delivered by goblet cells or M cells)
34
Q

what are the 2 main T cell differentiation pathways induced by DCs in the gut

A
  1. in the steady state - induce Treg cells (via TGF-beta) and Th2 –> quite suppressive cytokines
  2. under inflammatory conditions - may induce Th1 and Th17
35
Q

Main isotype switching of the gut and how

A

IgA via TGF-beta signal 3

36
Q

how do T and B cells find there way to mucosal tissue

A

DCs induce mucosal epithelial addressin alpha4beta7 on activated T and B lymphoyctes –> bind the MAdCAM1 integrin on vascular endothelial cells of all mucosal surfaces and chemokine receptors for the lamina propria

37
Q

What happens when activated T and B cells enter the lamina propria

A
  • activate B cells –> predominantly IgA
  • CD4 T cells (either regulatory Treg/Th2 in steady state or inflammatory Th1 and Th17)
  • CD8 T cells - protect against intracellular infections
  • many persist as memory cells
38
Q

how do the intestinal microflora interact with the gut immune system (general 4 things)

A
  • mucous layer
  • intestinal epithelial cells
  • development of lymphoid structures
  • development of lymphocyte subsets
39
Q

which PRRs are expressed on enterocytes and where are the located

A
  • TLR 2 and 4 - apical
  • TLR 3, 7 and 9 - in endosome
  • TLR 5 - expressed on baso-lateral surface
40
Q

Direct effects of microbiota on mucous layer and gut epithelium

A

block binding sites
produce bacteriocins
(Inhibit pathogen binding)

41
Q

indirect effects of microbiota on mucous layer and gut epithelium

A

interact with PRRs on enterocytes
SCFA effects
IL22 effects

42
Q

PAMP signalling via microbiota on enterocytes stimulates…

A
  • mucin production
  • proliferation of crypt enterocytes and Paneth cells
  • release of antimicrobial peptides
  • induction of regulatory cytokines (TGF-beta, IL-10)
43
Q

how does the SCFAs produced by the microbiota affect the mucous layer and gut epithelium

A

inhibit NF-KB and the production of other inflammatory cytokines

44
Q

development of Peyers patches, mesenteric lymph nodes and ILFs

A

peyers patches and mesenteric LN develop prenatally

ILFs develop post natally

45
Q

what initiates the development of ILFs

A

signalling by microbiota

46
Q

why do Peyers patches enlarge after birth

A

microbes of the microbiota enter via M cells and initiate further development

47
Q

difference between response of the body to microbiota and pathogens

A

normal microbiota - induce physiological inflammation (without damage to the host)
pathogens - induce pathological inflammation (damages the host)

48
Q

how does the gut discriminate between microbiota and pathogen in general

A
  1. position and number of the bacteria
  2. detect invasion
  3. differential interaction with PRRs
49
Q

what is the difference between microbiota and pathogen in regards to position and number

A

commensals found at the luminal edge of the mucous layer

pathogens bind tightly to invade the epithelial surface due to adhesins, invasins etc

50
Q

how does the gut epithelium detect invasion

A
  • TLR5 (at basolateral surface) activated

- damage via ROS and RNS detected by intracellular PRR

51
Q

how does the gut epithelium discriminate the different interactions of PRRs of microbiota and pathogen

A

inflammasome signalling

Type 3 secretion systems

52
Q

what is kwashiorkor

A

severe form of acute undernutrition

53
Q

how does the microbiota influence kwashiorkor

A

dysbiosis of microbiota affects the risk for kwashiorkor

54
Q

what is the hypothesis role of gut microbiota and nutrition

A

gut microbiota provides genes necessary for healthy growth and development

55
Q

what does Kwashiorkor microbiota do?

A

generates chemical products that result in selective inhibition of TCA cycle enzymes –> effect on energy metabolism

56
Q

high fat diets/obesity is associated with what kind of microbiota

A

a decrease in diversity of microbiota - number of bacteria are the same but just less diverse

57
Q

what is the connection between microbiome and T2DM

A

those with T2DM have an altered and PREDICTABLE microbiome

58
Q

individuals with low microbial diversity of their microbiome have what?

A

higher levels of insulin resistance, serum triglycerides, cholesterol and insulin

59
Q

how is obesity associated with low grade chronic infection

A

causes increased intestinal permeability –> activates more PRRs: causing:

  • induction of inflammatory cytokines (TNF-alpha, IL-1, IL-6 and IL-17)
  • increase in mast cells, T cells and macrophages
60
Q

what can the chronic low grade inflammation of obesity lead to

A

densensitisation of the insulin receptor and leptin receptor signalling

61
Q

what causes inflammatory bowel disease

A

elevated immune responses against intestinal microflora

62
Q

what is the bacterial diversity of people with IBD

A

bacterial diversity is reduced

63
Q

intestinal permeability in people with IBD is increased or decreased?

A

increased

64
Q

what is the current theory about why people with IBD start to make immune responses against their microflora

A

defective signalling through PAMP-PRR interactions leads to persistence of microorganisms and their products resulting in persistent invasion –> leading to recurrent or chronic inflammation
(instead of physiological inflammation –> chronic pathological inflammation)

65
Q

how is the microbiome associated with the development of allergies

A

Postulate the pre and postnatal microbial interactions very early in childhood by certain commensals signal for differentiation to a regulatory phenotype

66
Q

what are the bacteria associated with allergic atopy?

A

higher incidence of Clostridia

low levels of Bifidobacteria

67
Q

alteration of microbiota can cause which types of GIT disease

A
  • susceptibility to GI pathogens
  • overgrowth of Candida –> diarrhoea
  • overgrowth of Clstridium difficile –> pseudomembranous colitis
68
Q

what kind of bacteria is Clostridium difficile

A

gram positive, anaerobic, spore forming, rod

69
Q

how does an overgrowth of Clostridium difficile cause pseudomembranous colitis

A

adheres to mucosal epithelium and produces cytotoxic toxins that cause cell death, inflammation and bowel necrosis

70
Q

treatment of Psuedomembranous colitis

A

metronidazole +/- vancomycin

71
Q

patients with recurrent Clostridium difficile infections posses microbiota characterised by

A

reduced diversity

72
Q

treatment of recurrent C. difficile pseudomembranous colitis

A

faecal transplant!!

Z MD1 GI block (18 decks)

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