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MSN 6204 GI Final > Eubiosis and Dysbiosis > Flashcards

Eubiosis and Dysbiosis Flashcards

1
Q

Human GIT microflora contains how many viable microorganisms?

A

10 to the 14 power from over 1000 species; 100 x that of human body cells

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2
Q

Three Main Enterotypes of microflora?

A

 Bacteroides (enterotype 1)
◦ associated with diets rich in animal protein and
saturated fats
 Prevotella (enterotype 2)
◦ associated with a predominantly plant-based diet
 high in carbohydrates & low in meat and dairy
 Ruminococcus (enterotype 3)
◦ originally believed as most prevalent, now appears
least prevalent (Guinane & Cotter, 2013

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2
Q

Three Main Enterotypes of microflora?

A

 Bacteroides (enterotype 1)
◦ associated with diets rich in animal protein and
saturated fats
 Prevotella (enterotype 2)
◦ associated with a predominantly plant-based diet
 high in carbohydrates & low in meat and dairy
 Ruminococcus (enterotype 3)
◦ originally believed as most prevalent, now appears
least prevalent (Guinane & Cotter, 2013

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3
Q

What are the health benefits of the colonic microflora?

A
  1. Enhanced GIT motility & function
  2. Modulate the immune system
  3. Improved digestion and nutrient
    absorption
  4. Production of Vitamins
    ◦ B group
    ◦ Vitamin K
  5. Xenobiotic metabolism
  6. Colonisation resistance
    ◦ ‘the protection against colonisation of the intestinal
    tract with potentially pathogenic bacteria afforded by
    the intestinal flora
  7. Production of SCFAs
  8. Production of polyamines
     polyamines (putrescine, spermidine, and spermine)
    participate in a large number of cellular processes, such
    as:
     cell growth and differentiation
     regulation of RNA, DNA and protein synthesis
     improve GIT microcirculation
     can be utilised as an instant energy source by intestinal cells
  9. Weight management
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4
Q

Physiological Activity of SCFAs

A

◦ 3 main SCFAs
 butyrate, propionate, acetate
◦  colonic pH
◦ improves colonic epithelial barrier function
mainly from butyrate
◦ protect against colon carcinogenesis
◦ have trophic effects on small intestine
◦ improve laxation
◦ improve circulation to colon and liver
◦ improve mineral absorption
◦ decrease colonic and systemic inflammation

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5
Q

What is the pH and microbial biomass along the GI tract, mouth, stomach, duodenum, jejunum, ileum, colon

A

Mouth: 100 million to billion cells/ml
Stomach: pH 1.5-5; 100-1000 cells/ml
Duodenum: pH 5-7; 1000-10,000 cells/ml
Jejunum: pH 7-9; 10,000 - 100,000 cells/ml
Ileum: pH 7-8; 100 million cells/ml
Colon: pH 5-7; 100 billion cells/ml

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6
Q

In what ways does the colonic microflora modulate the immune system?

A
  1. GIT flora promotes secretion of intestinal secretory IgA

2.shift T-helper cell balance towards Th-1
  production of IgE and eosinophils
 dampens hypersensitivity reactions and intestinal inflammation
 induces oral tolerance
 prevents development of atopic diseases

  1. may modify antigens to less antigenic forms
     induces & maintains oral tolerance

4.Non-specific immune stimulation
 in vitro - ↑ production of cytokines, tumor necrosis factor
α and interleukin 6 (reflecting stimulation of nonspecific
immunity)
 Increases production of macrophages and stimulates
phagocytosis

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7
Q

How colonic microflora enhances GIT motility and functions?

A
  1. gastric emptying, small intestinal transit, and colonic
    transit have all been found to be more rapid in
    conventional animals than in their germ-free
    counterparts
  2. ‘normal’ GIT propulsive activity is determined to a
    significant degree by the presence of the normal flora
     microbial production of nitric oxide, short-chain fatty acids, and polyamines may play a role
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8
Q

How does colonic microflora improve digestion and nutrient absorption?

A
  1. provides about 10% of daily energy needs via fermentation in colon
  2. salvages energy from unabsorbed carbohydrates
    in the colon → SCFAs
  3. improves the absorption of calcium, magnesium
    and trace minerals
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9
Q

Colonic microflora produces which vitamins?

A

B group, K
- note: high dose abx&raquo_space; to vit K deficiency&raquo_space; incr risk of clots

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10
Q

The colonic microflora produce polyamines. What do they do for health?

A

 cell growth and differentiation
 regulation of RNA, DNA and protein synthesis
 improve GIT microcirculation
 can be utilised as an instant energy source by intestinal cells

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11
Q

How are colonic microflora related to weight management?

A

microflora plays a vital role in energy
homeostasis
 obese microbiota has an increased capacity to
harvest energy from the diet

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12
Q

Define “dysbiosis”

A
  1. ‘qualitative and quantitative changes in the
    intestinal flora, their metabolic activities or their
    local distribution that produces harmful effects on
    the host
  2. growth of potentially pathogenic microorganisms
    over their beneficial counterparts and/or alterations
    in the metabolic activities of the flora
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13
Q

Dysbiosis plays role in what chronic/degen diseases?

A

e.g., rheumatoid arthritis, ankylosing
spondylitis, IBS, IBD, atopic eczema, obesity

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14
Q

How does microflora of IBS patients differs from
that of healthy controls?

A

◦ lower faecal concentrations of bifidobacteria and
lactobacilli
◦ higher concentrations of Enterobacteriacea

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15
Q

How is dysbiosis presented in ulcerative colitis?

A

  colonic concentration of lactobacilli
 toxic strains of Escherichia coli may play a role
  populations of Faecalibacterium prausnitzii
 95% of UC sufferers are colonised by sulphate-reducing
bacteria (SRB)
 active UC is associated with  production of luminal hydrogen
sulphide

16
Q

How is dysbiosis presented in Crohn’s Disease?

A

  in faecal bifidobacteria
 toxic strains of E. coli may play a role
 elevated numbers of Bacteroides spp.
  populations of Faecalibacterium prausnitzii

17
Q

How does Dysbiosis in Atopic Eczema present?
 Babies who later developed AE

A

◦ ↓ enterococci
◦ ↓ bifidobacteria
◦ ↑ clostridia
◦ ↑ Bacteroides spp.
◦ ↑ E. coli

18
Q

How does dysbiosis incr risk of kidney stones?

A

Presence of colonic Oxalobacter formigenes
(OF) reduces the risk of kidney stones (Kaufman et
al, 2008)
◦ OF utilise oxalate as sole food source
 thereby decreasing amount of oxalate available for
absorption
◦ After triple antibiotic therapy (Kharlamb et al, 2011)
 of subjects who were OF positive at baseline, only 37%
continued to be colonised by OF after 1 and 6 months

19
Q

How does dysbiosis present in obesity?

A

◦ obese people have:
 lower Bacteroidetes and more
Firmicutes than lean subjects (Ley et al,
2006)
 higher proportion of gram-negative
bacteria in the microflora

Infant antibiotic exposure is a risk factor
for childhood obesity

20
Q

Causes of dysbiosis?

A
  1. Antibiotics
  2. Chemotherapy
  3. Stress
  4. Cesarean section
  5. birth location (hospital vs home)
  6. Formula feeding
  7. Diet
21
Q

What dietary patterns are assoc with dysbiosis?

A

 sulphates and sulphites
 high protein diets
 high animal protein diets
 high fat diets
 high in refined carbohydrates

22
Q

Products of protein putrefaction in the colon?

A

SCFAs
BCFA
Phenols and Indoles - co-carcinogens
Ammonia - mutagen, cellular poison
Amines: neurotransmitter and mutagen precursors
HS and thiols: cellular toxins

23
Q

high protein diet and dysbiosis changes?

A

 Induces changes to the ecosystem: (Duncan et al, 2007)
◦ Decreases in faecal concentrations of bifidobacteria
 50% decline on a high-protein + low-carb diet in
just 4 weeks!
◦ Decreases in concentrations of butyrate-producing species
 Roseburia spp. and Eubacterium rectale
◦ Decreases in faecal butyrate

24
Q

How does high animal protein diet&raquo_space; dysbiosis?

A

Diets high in animal protein →  activity of certain
bacterial enzymes, such as beta–glucuronidase,
azoreductase, nitroreductase and 7--hydroxysteroid
dehydroxylase →  release of potentially toxic and
unwanted metabolites in the bowel
 can be attenuated through prebiotic
consumption

25
Q

HIgh fat diet and dysbiosis?

A

◦ increases in the ratio of gram-negative to gram-positive (Cani et al, 2008)
 e.g., an increased proportion of lipopolysaccharide-containing microbiota
in the gut
 greater pool of luminal endotoxin
 LPS represents ~80% of the cell wall mass of gram-negative bacteria
◦ decreases in bifidobacteria concentrations (Cani et al, 2007)
◦ increases in E. coli populations (Martinez-Medina et al, 2013)
◦ increases in Desulfovibrionaceae (Hildebrandt et al, 2009)

Meals high in fat increase endotoxin absorption (Laugerette
et al, 2011)
 → postprandial endotoxaemia → low-grade systemic inflammation
◦ the higher the fat content the higher the serum level of
endotoxins
◦ saturated fat appears to further enhance endotoxin
absorption (Mani et al, 2013)
 whereas omega-3 fats attenuate postprandial endotoxaemia
◦ concurrent consumption of fibre (30g) also
attenuates postprandial endotoxaemia

26
Q

Diets High in Milk Fat and dysbiosis?

A

Animal models have found that ingesting increased
amounts of milk fat (but not safflower oil) triggers
blooms of an otherwise rare gram-negative
bacterium – Bilophila wadsworthia
◦ went from nearly 0% of flora to 6%
◦ B. wadsworthia consumes sulphur-rich bile salts
produced to help breakdown the milk fat
 → ↑ in H2
S production and gut inflammation

27
Q

sucralose and dysbiosis?

A

◦ Causes significant changes in the microflora
 Reductions in:
 total anaerobes
 total aerobes
 beneficial bacteria:
 bifidobacteria
 lactobacilli

◦ Increased faecal pH

28
Q

how is dysbiosis diagnosed?

A
  1. Primarily based on the patient’s medical and diet
    history
    * recent history of antibiotic use, or multiple
    courses of antibiotics; recent chemotherapy or
    radiotherapy; long-term PPI or NSAID use
    * suffer from one or more of the diseases detailed
    earlier
    * high stress levels
    * dietary risk factors
    * SAD; Ketogenic diet; High fat-low carb; high
    protein-low carb; high processed carb; low
    fibre diets; low FODMAP diet; diets low in
    plant food diversity
  2. Specialised stool testing
29
Q

Stool Test Summary

A
  • Culture has no role to play in assessing GI microbiota
    composition – so don’t use it!
  • Most accurate and comprehensive results come from
    combining a molecular stool test using 16s RNA or shotgun
    metagenomic sequencing with a CDSA/CSA (complete digestive stool analysis/comprehensive stool analysis)
  • broad overview of ecosystem and diversity scoring
  • all important genera highlighted and more!
  • microbe metabolic pathways (shotgun only)
  • digestive & microbial markers – faecal fat, pancreatic elastase, stool
    pH, total SCFAs & ratios, β-glucuronidase
  • inflammatory & immune markers – calprotectin, sIgA, mucous,
    lactoferrin, occult blood
  • however – ignore the microbe section on culture-based CSAs/CDSAs!
30
Q

Tools used to treat dysbiosis?

A

 Prebiotics
 Probiotics
 Colonic foods
 Antimicrobial herbs?

31
Q

What probiotics to use for dysbiosis?

A

 Bifidobacterium lactis HN019 (Ahmed et al, 2007)
◦ increases in faecal concentrations of
bifidobacteria (P<0.0005), lactobacilli (P<0.005),
and enterococci (P<0.005) compared to baseline;
◦ decrease in coliforms (P<0.005)
 Lactobacillus rhamnosus GG (Benno et al, 1996)
◦ increases in faecal concentrations of
bifidobacteria and lactobacilli (both P<0.05)
◦ decrease in clostridia concentrations

32
Q

Define colonic foods?

A

foods entering the colon and serving as
substrates for the endogenous colonic
bacteria, thus indirectly providing the host
with energy, metabolic substrates and
essential micronutrients.

33
Q

Colonic foods for dysbiosis examples?

A

*Brown rice
*Carrots
*Cocoa
*Green tea

34
Q

General Dysbiosis Treatment
Approaches

A

General Dysbiosis Treatment
Approaches
 Selective Weeding - if deemed necessary,
choose selectively-acting antimicrobials first
before using broad-spectrum options
◦ Garlic
 preferably raw
◦ Green tea extract
 ~300mg catechins/day
◦ Pomegranate husk

35
Q

General Dysbiosis Treatment
Approaches

A

 Leave more broad-acting, potentially
microflora-damaging options as last resort
◦ Berberine-rich herbs
 Coptis chinensis (10% in 1:2 tincture)
 Phellodendron amurense (6%)
 Hydrastis canadensis (3%)
 B. vulgaris and M. aquifolium too low in berberine to have
significant impacts as antimicrobials
◦ Enteric-coated essential oils
 Oregano, thyme, clove, cinnamon
◦ Antibiotics
Would you p

MSN 6204 GI Final (21 decks)

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