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MMI 436 > IBD > Flashcards

IBD Flashcards

1
Q

What is IBD?

A

a spectrum of remitting and relapsing chronic inflammatory conditions of the intestine

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2
Q

What is the difference between CD and UC?

A

CD

  • patchy and transmural inflammation anywhere in the GI tract from mouth to anus

UC

  • continious superfifical inflammation starting from the anus and works its way up
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3
Q

Does living in rurual/being exposed to greenspaces or urban areas reduce the risk of IBD? Which age group is this important for?

A

growing up in a rurual environment or being exposed to greenspaces during the first five years of life was associated with a reduced risk of IBD

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4
Q

What kind of countries have higher prevelances of IBD?

A

industrialized countries – especially western socieity

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5
Q

How does immigration affect the risk of IBD? What does this suggest?

A
  • younger age at time of immigration association with highest risk
  • next generation assumes risk of general population
  • suggests some environmental exposure during early period of life can predispose individual to developing IBD
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6
Q

How can microplastics be ingested during infant formula prep?

A

formula prep promotes the release of microplastics from polypropylene bottles

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7
Q

What is IBD characterized by?

A

a dysregulated immune response – more pro- than anti-inflammatory

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8
Q

What kind of genes are associated with risk of IBD?

A
  • microbial sensing
  • microbial clearance
  • epithelial barrier
  • integration of antimicrobial adaptive responses
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9
Q

How deos the microbiota regulate human health?

A
  • educates the IS
  • aids in digestion of plant material
  • produces energy substrate for HCs (SCFA)
  • produces vitamins and antimicrobials
  • produces signalling molecules to interact with immune and epithelial cells
  • communicates with brain
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10
Q

what phyla of bacteria promotes health vs disease? In a low biodiversity microbiome which kind of bacteria is there more of?

A

health = bacteriodetes, firmicutes
disease = proteobacteria, fusobacteria (e.g. E coli)

less biodiveristy –> more proteobacteria and fusobacteria

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11
Q

What factors affect gut microbiota composition and function?

A
  • exercise
  • stress
  • antibiotics
  • age – biodiversity decreases when aging
  • diet – breast milk vs. formula
  • mode of birth delivery
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12
Q

Does your small intestine or large intestine have more bacteria?

A

large intestine

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13
Q

Why does the mucosal IS have to be balances between immune activation and suppression?

A
  • immune activation for protection from pathogens (e.g. has to protect against salmonella)
  • immune suppression (tolerance) to allow for peaceful co-existence with commensal microbes
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14
Q

What are microbial bar codes?

A

each microbe has its unique set of Ags which will activate different sets of TLRs which will lead to different responses

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15
Q

What are the five barriers of the gut against pathogens?

A
  1. microbial layer (commensal bacteria)
  2. chemical barrier (mucus layer)
  3. physical barrier (the epithelium + tight junctions)
  4. immunological barrier
  5. muscle layer
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16
Q

Describe the polarized expression of TLRs on intestinal epithelial cells (IECs), why is this important?

A

no TLR4/5 on the apical (lumen) side, expressed on the basolateral surface

activated by bacterial flagellin – if bacteria are in the lumen, thats fine; if bacteria on the basolateral side, that bad so need to trigger an immune response

17
Q

What cytokines do epithelial cells release when activated? What do they do?

A

IL-6, IL-1B –> polarizes T cells into Th1 phenotype – proinflammatory response

18
Q

During homeostasis of the gut, what signals do IECs release to DCs to maintain tolerance, and what signals do DCs release to Tregs cells to maintain tolerance to microbes?

A

IEC –> DC

  • TSLP
  • IL-10
  • TGFB
  • RA

DC –> Treg

  • RA
  • TGFB
19
Q

A dysfunctional mucosal immune response is the central driver of IBD, what is it characterized by?

A
  • altered innate immunity
  • activated effector T cells
  • large presence of B cells and Ab production
  • large recruitment of ICs from circulation
  • large production of pro-inflammatory mediators
20
Q

What is the GEM study?

A

international study that started in 2008 that is following 5000 subjects that are”at-risk” of developing CD (1st degree relatives of those with IBD)

21
Q

What kind of microbial changes are commonly seen in IBD patients?

A
  • less microbial diversity
  • less commensal bacteria
  • more bacteria that break down the mucus layer
  • less bacteria that produce butyrate and propinoate (SCFA)
22
Q

Why are SCFAs important?

A
  • energy source of coloncytes
  • stimulate mucus production
  • induce Treg cells
  • enhance CD8 T cell responses
  • stimulate sIgA production
  • enhance epithelial barrier function
  • more AMPs
23
Q

Why are ROS bad for the gut?

A

ROS kills butryate producing microbes and E.coli loves oxygen

24
Q

What happens if you transfer dysbiotic microbiota to healthy mice?

A

certain strains of bacteria can transfer the colitis phenotype

25
Q

What (4) host deficiencies can prevent containment of commensal bacteria?

A
  1. less mucus secretion (less expression of the MUC1 gene)
  2. increase gut permeability (altered expression of tight junction proteins; driven by dietary factors)
  3. decreased AMP secretion
  4. worser ability to kill bacteria
26
Q

How does the LOF NOD2 gene affect chronic inflammation?

A

NOD2 fails to recognize and properly deal with commensal bacteria –> intestinal inflammation (NOD1/2 detect peptidigylcan)

27
Q

What are the treaments for IBD?

A
  • surgery
  • biologic agents
  • immunomodulators
  • antibiotics
28
Q

What is the cascade effect?

A

cytokines can stimulate production of other cytokines

29
Q

What are biologic drug targets?

A
  • cytokine blockade (block cytokine receptors)
  • intracellular signaling pathway blockade
  • cytokine targeting
  • lymphocyte trafficking blockade
30
Q

What would personalized treatment take into consideration to determine an appropriate treatment?

A
  • genome
  • transcriptosome
  • microbiome
  • cellular measurements

MMI 436 (14 decks)

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