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Probiotics > Module 16 > Flashcards

Module 16 Flashcards

1
Q

Congenital Lactose Intolerance

A

Deficiency in b-galactosidase

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2
Q

B-galactosidase

A

Digestion of disaccharide lactose

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3
Q

Lactose Intolerance Help

A

Intake of fermented dairy instead of milk so LAB produce B-galacotsidase to breakdown lactose in intestine or milk

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4
Q

B-galactosidase not function

A

Lactose makes CS of intestine secrete water into intestine and lots of bacterial fermentation –> Production of H, CO2, lactic acid, and acetic acid –> loose stool, bloating, abdominal pain, flatulence

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5
Q

Types of Diarrhea Treatments

A

Infantile, Antibiotic-associated, Traveller’s

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6
Q

Infantile diarrhea

A

Several viruses and bacteria but mainly rotavirus

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7
Q

Leading cause of acute viral gastroenteritis in children

A

Group A Rotavirus (GVA) at about 440,000 deaths/year

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8
Q

GVA Mechanism

A

Enhanced permeability of gut epithelial cells to intact proteins and altered handling of antigens in enteric route

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9
Q

Steps of RVA

A

Increased permeability of intestinal wall –> More antigens across barrier –> Bigger inflammatory response

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10
Q

Why probiotics might help with GVA

A

Enhance mucosal integrity

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11
Q

GVA in animal models

A

Rodents and Pigs

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12
Q

Bacteria against RVA

A

Lactobacilli casie sp. rhamnosus strain GG and Bifidobacteria bifidum

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13
Q

Antibiotic-Associated Diarrhea

A

Otherwise unexplained diarrhea that occurs in association with antibiotics

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14
Q

Pseudomembranous colitis

A

C. diff etiological agent

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15
Q

Most common cause of antibiotic-associated diarrhea

A

C. diff

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16
Q

Antibiotics…

A

Disrupts barrier function of normal microbiota so C. diff can establish itself and produce toxin

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17
Q

Antibiotics for C. diff

A

Metronidazole and Vancomycin with recurrence common

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18
Q

Probiotics Prevention of C. diff

A

Conflict with B. longum superior to placebo for erythromycin induced diarrhea in 10 healthy and L. GG having lower incidence compared with yogurt placebo

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19
Q

Probiotic for C. diff

A

Lactobacillus GG

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20
Q

Treatment for C. diff times

A

Ongoing infection or while on antibiotics

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21
Q

Psuedomembraneous colitis mechanism

A

Exaggerated response of circulating neutrophils and monocytes due to toxin –> inflamed intestinal tissue and cell death

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22
Q

Traveler’s diarrhea

A

Many microbes but most caused by enterotoxigenic E. coli from drinking water in different countries

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23
Q

Results of probiotics in TD

A

Conflict depending on strain, vehicle, and dosage (hard to evaluate)

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24
Q

Prevalence of H. pylori gastritis

A

50% worldwide

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25
Q

Chronic gastritis

A

H. pylori

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26
Q

Increased risk of peptic ulcer disease

A

H. pylori

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27
Q

Increased H. pylori cancers

A

MALT lymphoma and Gastric Cancer

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28
Q

Probiotics for H. pylori

A

Improve eradication with other anti-therapies and decrease antibiotic related side effects

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29
Q

Mechanisms that treat H. pylori

A

(1) AM substance production
(2) Epithelial cell adhesion and competition
(3) Mucosal barrier stabilization
(4) IR regulation
(5) sIgA secretion

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30
Q

AM substance production to treat H. pylori

A

Bifidobacterium and Enterococcus generate heat stable protein

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31
Q

Mucosal barrier stabilization

A

Tight junction strengthened so pathogen cannot get through

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32
Q

Immune response regulation for H. pylori

A

Probiotics stimulate –> pathogen gets there –> quick IR to clear

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33
Q

First line of tolerance

A

sIgA Secretion

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34
Q

For H. pylori treatment

A

Combo of probiotics more effective in eradication or big proportion elimination

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35
Q

Necrotizing Enterocolitis (NEC)

A

Acute inflammation due to immature intestine that effects 5-10% of low birth rate infants

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36
Q

NEC leads to…

A

High mortality, heavy complication, invalidating sequelae

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37
Q

Immaturity of Intestinal barrier

A

Likely major etiological factors of NEC

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38
Q

Probiotics of NEC

A

Any microbe can invade so any bacteria that can strengthen the intestinal barrier

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39
Q

Most probiotic trials on NEC

A

Focus on impact of intestinal colonization measured by fecal microbiota composition analysis

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40
Q

Probiotics for NEC

A

Variety or mix of strains or synbiotics reduce level of pathogenic bacteria and yeast

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41
Q

L. reuteri ATCC 55730

A

Accelerate GI motility to prevent bacterial overgrowth in NEC

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42
Q

B. lactis SNSM I-33446

A

Faster decrease of intestinal permeability levels in NEC –> preterm barrier function

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43
Q

Most trials on NEC focus on

A

Microbiota to determine if it’s the agent of disease

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44
Q

IBS

A

GI disorder characterised by association between recurrent abdominal pain/discomfort and change in stool consistency and frequency

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45
Q

IBS categories by symptoms in subgroup

A

Constipation-predominant, Diarrhea-predominant, Mixed type

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46
Q

IBS Cause

A

Deregulated IR directly related to deterioration of intestinal barrier function

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47
Q

Microbiota in IBS

A

Debate but microbiota likely involved in disease symptoms

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48
Q

How microbiota contributes to IBS

A

(1) Altered fermentation
(2) Harmful modulation of enteric sensorimotor function
(3) Impair intestinal barrier function
(4) Sustained Immune activation without macroscopic signs of inflammation
(5) Harmful modulation of the brain-gut axis

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49
Q

IBS symptom score probiotics

A

Those that increase barrier function

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50
Q

IBS has

A

Lots of scientific debate

51
Q

Chicken or egg approach for

A

Microbiota causing intestinal barrier disruption in IBS or otehr way

52
Q

Disruption of barrier causes

A

Inflammation and sustained IR

53
Q

IBS probiotic studies

A

Mostly in vitro and ex vivo cell culture + animal models such as mice and rats

54
Q

IBS studies work by

A

Disrupting the intestinal barrier before adding probiotic strain or a mixture

55
Q

Probiotics in IBS can lead to…

A

Alleviation of symptoms in animals + restoration of barrier function by enhancing tight junction proteins

56
Q

Tight junction proteins

A

Occludin, E-cadherin, Claudin-1

57
Q

Tight junction proteins produced to help

A

IBS to enhance barrier function

58
Q

Lost of probiotics and mixtures tested

A

IBS

59
Q

IBD overall term to describe

A

CD and UC and Pouchitis

60
Q

Affect any part of bowel but predominately terminal ileum and colon

A

Chron’s Disease

61
Q

Granulomatous, patchy, transmural mononuclear inflammation

A

CD

62
Q

Only affects the colon

A

UC

63
Q

Lesions mucosal and continuous

A

UC

64
Q

UC

A

Massive neutrophil infiltration, crypt abscesses, loss of goblet cells, epi damage

65
Q

Acute or chronic inflammation of ileal reservoir

A

Pouchitis

66
Q

Pouchitis

A

After colectomy and ileal pouch-anal anastomosis following UC

67
Q

Active IBD

A

Mucosal inflammation + impaired barrier function

68
Q

Remission of CD and UC Requires

A

Immunosuppressive agents such as corticosteroids, azathioprine, and anti-TNF

69
Q

Probiotics not tested on

A

Active IBD

70
Q

Probiotics in IBD

A

Maintaining remission

71
Q

Probiotics for IBD Treated for…

A

Pouchitis mostly, some UC, unlikely CD

72
Q

Probiotics in constipation

A

Reduce whole gut transit time and increased stool frequency

73
Q

Probiotic microbes in constipation

A

Bifidobacterium lactis but not L. casei Shirota

74
Q

Cancer prevention and proboitics

A

Changes related to tumor induction and promotion

75
Q

Cancer prevention mechanisms

A
  1. Alter intestinal microecology (microbiota effect)
  2. Altered intestinal metabolic activity
  3. Normalize intestinal permeability
  4. Enhanced intestinal immunity
  5. Strengthened intestinal barrier mechanisms
76
Q

Altered Microecology (Microbiota effect)

A

Remove from the microbiome microbes that have ability to turn pro-carcinogens to carcinogens

77
Q

Cancer prevention mostly…

A

Removal of cancer promoting compounds or inhibition of transformation of non-carcinogens into carcinogens

78
Q

Strengthen intestinal Barrier through

A

Altering microecology + Altered metabolic activity + normalize intestinal permeability + enhance intestinal immunity

79
Q

Specific Examples of LAB in Cancer prevention

A

(1) Bind mutagenic amines generated when cooking protein rich food
(2) Degrade nitrosamines
(3) Reduce activity of bacterial B-glucuronidaes, nitroreductases, adn azoreductases
(3) Inhibit quinoline (IQ) induced incidence of colon tumors in rats
(4) Bind aflatoxins (fungal endotoxins that are pro-carcinogens) so they cannot be adsorbed by the intestine

80
Q

2-amino-3-methylimidazol [4,5-f] quinoline (IQ)

A

Induce intestinal tumors

81
Q

Detrimental to dental health

A

Sugar fermentation and pH decreases + high buffering capacity of milk products and calcium concentrations that help in protection of dental surfaces

82
Q

Preventative effect of fermented milks and cheeses

A

Lactobacillus GG colonize oral mucosa and prevent growth of S. sorbinus + S. mutants

83
Q

Nutritional absorption + Specialized barrier function

A

Intestinal mucosa

84
Q

Front line of intestinal barrier

A

Single layer of specialized epithelial cells linked together by tight junction proteins (TJ)

85
Q

Factors that support intestinal barrier

A

Mucins, AM molecules, Immunoglobulins, cytokines

86
Q

Enterocytes

A

Specialised epithelial cells of the intestine that form single barrier with tight junctions

87
Q

Leaky gut

A

Barrier factor abnormalities causes intestinal permeability

88
Q

Paneth Cells

A

Secrete antimicrobial molecules

89
Q

Goblet Cells

A

Produce mucus

90
Q

Lamina propria

A

Layer right under epithelial cells that has cells that sense the exterior or secrete IgA with AM activity

91
Q

Leaky gut problems

A

Microbes or toxins get accross –> exaggerated IR

92
Q

Leaky gut leads to

A

Autoimmune diseases due to antigens entering the gut lumen –> local and systemic immune responses

93
Q

Diseases arise or exacerbated due to leaky gut

A

IBD, Celiac disease, Autoimmune hepatitis, T1D, MS, SLE

94
Q

Requirements for gut derived systemic IR

A

TLR activation + inflammasome stimulation + Dysbiosis + Molecular mimicry + Breech of barrier

95
Q

Inflammasome

A

Protein complexes in different cells that induce secretion of IL1B and IL-18

96
Q

Molecular mimicry

A

Antigens similar to our own is original target for the IR so antibodies get directed against our own cells

97
Q

Chronic immune-mediated inflammatory liver disease with uncertain cause

A

Autoimmune Hepatitis

98
Q

Susceptibility factor of autoimmune hepatitis

A

MHC

99
Q

Key antigen targets for autoimmune hepatitis

A

Cytochrome P450 2D6 (CYP2D6) + formiminotransferase cylcodeaminase

100
Q

Molecular mimicry example

A

CYP2D6 and HCV, HSV, CMV –> autoimmune hepatitis

101
Q

Steps to AI Hepatitis

A

Dysbiosis of intestine –> bacterial ligands and toxins get into bloods stream –> to liver through portal veins –> activate T-cells –> exacerbate responses or activation of inflammasome –> Inflammation, liver damage, hepatic fibrosis

102
Q

AI associated with…

A

Dysbiosis evidenced by proteins binding intestinal epithelial cells being reduced in patients with A disease + LPS increased + decreased intestinal anaerobes (Bifidobacterium and Lactobacillus)

103
Q

Structural proteins reduced in AI hepatits

A

Zona occludens 1 and occludin

104
Q

AI and probiotics

A

Not addressed yet due to no animal model

105
Q

Severe persistent inflammation that leads to tissue damage of multiple organs

A

Systemic Lupus Erythematosus

106
Q

Women are … more likely to get SLE

A

9x

107
Q

SLE characterised by

A

Autoantibodies, auto reactive T-cells, Abnormal generation of proinflammatory cytokines

108
Q

Therapeutic for SLE include

A

Restoring imbalanced cytokines and deficient immune cells

109
Q

Triggers of SLE

A

Genetics, environment, unknown –> activation of IR against self Ag –> auto reactive B cells, pro cytokines, and inflammatory T cells

110
Q

Inducers of SLE

A

LPS penetrated intestinal epithelium and translocating to tissues

111
Q

Spontaneous development of lupus in mice

A

TLR4 increased induced by LPS

112
Q

Treatment of SLE

A

Antibiotics to rid of commensal gut flora + Immunoregulatory probiotics

113
Q

Immunoregulatory probioitcs

A

Enhance Treg cells and control inflammatory response –> induce tolerance

114
Q

Before T1D disease onset

A

Impaired intestinal barrier functions (microbiome trigger)

115
Q

Pancreatic B cells

A

Destroyed by autoimmunity in T1D

116
Q

Zonulin

A

Pathogenic role of intestinal permeability in T1D depended on it; relies on bacterial colonization

117
Q

Bacteria to T1D

A

Bacterial colonization –> Zonulin colonization –> increased intestinal permeability –> pathogenesis

118
Q

Zonulin inhibitor in rats

A

Reversion of intestinal barrier dysbiosis relives symptoms of T1D

119
Q

T1D faucets

A

Altered microbiota + leaky gut + altered mucosal immunity

120
Q

T1D perfect storm

A

Altered microbiota —> exacerbated IR because increased presentation of antigen to APCs that get through the leaky gut —> T-cells activation —> cytokine relasesa nd secretion of autoantiboides in pancreas —> perfect storm because everything must act together for autoimmune reaction

121
Q

Contributes to T1D development

A

Microbial Translocation

122
Q

Streptozotocin-induced T1D

A

Gut bacteria able to translocate into PLNs and contribute to T1D + had a distinct microbiota

123
Q

PLNs translocation proof

A

Treat streptozotocin mice with antibiotics –> PLNs sterile and disease attenuated

Probiotics (16 decks)

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