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BIOL3076 - Microbiomes and Health > FP - Gut Microbiome IBD > Flashcards

FP - Gut Microbiome IBD Flashcards

1
Q

What is Inflammatory Bowel Disease (IBD)? (2)

A
  • Chronic, relapsing, immune-mediated disorders of the GI tract
  • Multifactorial nature with gene-environment interactions and microbiome involvement
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2
Q

What are the 2 main forms of IBD?

A
  • Crohn’s disease (CD)
  • Ulcerative colitis (UC)
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3
Q

How can you distinguish Ulcerative Colitis (UC) from Crohn’s Disease (CD)? (8)

A

Ulcerative Colitis (UC):
* Distribution: Continuous, symmetric, diffuse
* Depth of Inflammation: Mucosal/submucosal
* Site: Colon only
* Rectal Involvement: Almost always involves rectum

Crohn’s Disease (CD):
* Distribution: Discontinuous, asymmetric, skipped segments
* Depth of Inflammation: Mucosal, submucosal, and/or transmural
* Site: May affect any part of the GI tract
* Rectal Involvement: Relative rectal sparing may occur

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4
Q

What trends are associated with the incidence of Inflammatory Bowel Disease (IBD)? (4)

A
  • Increased in the Western world since the Industrial Revolution
  • Accelerated further during the 1950s “Great Acceleration”
  • Rising in newly industrialized countries with globalization
  • Western lifestyle linked to higher IBD risk via immune modulation and microbiota changes
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5
Q

How does antigen exposure affect the microbiota in IBD? (2)

A
  • Leads to dysbiosis or selection of pathobionts
  • Microbiota changes drive IBD pathogenesis
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6
Q

What roles do immune cells play in IBD pathogenesis? (2)

A

IECs and SCs: Critical for immune surveillance
Tregs and Th17 cells: Regulate immune tolerance and activation

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7
Q

What genetic mechanisms underlie IBD? (4)

A
  • Barrier integrity loss: CDH1, MUC19
  • Paneth and goblet cell dysfunction: XBP1, ORMDL3
  • Innate immune activation loss: NOD2, ATG16L1, IRGM
  • Immune regulation loss: TNFSF15, IL-10RB, IL-23R
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8
Q

How does barrier integrity disruption contribute to IBD pathogenesis? (2)

A

Barrier integrity is disrupted at all levels, leading to chronic inflammation.

  • Microbiota changes: Dysbiosis or pathobiont selection drive inflammation.
  • Genetic susceptibility: Alters intestinal tissue and immune responses, promoting chronic inflammation.
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9
Q

What is dysbiosis and its role in disease? (3)

A
  • An alteration in microbiota community structure and/or function
  • Capable of causing/driving a detrimental distortion of microbe-host homeostasis
  • Specifically, it initiates or propagates disease
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10
Q

What microbiota changes are observed in twin cohorts with IBD? (5)

A

Crohn’s Disease (CD):
- Lower levels of Faecalibacterium and Roseburia
- Higher levels of Enterobacteriaceae and Ruminococcus
- Presence of adherent-invasive Escherichia coli (AIEC) in ileal lesions

Ulcerative Colitis (UC):
- Reduced species richness and alpha diversity
- Enrichment of Actinobacteria (Rhodococcus) and Proteobacteria (Shigella/Escherichia)

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11
Q

How do microbial effectors contribute to IBD pathogenesis? (6)

A

Nod2-deficient mice:
- Elevated commensal bacterial load
- Dysbiosis and reduced pathogen defense

Microbial effectors:
- Single or combined bacterial effectors can elicit pathogenesis
- Maintain barrier function for intestinal homeostasis

IL10-/- model:
- Colitis depends on enteric bacteria (e.g., Enterococcus faecalis)
- Attenuated with ΔepaB (antigen) or Δlgt lipoprotein mutants

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12
Q

How does diet influence microbiota and immune response during inflammation? (5)

A

High saturated fat diet:
- Alters microbial assemblage conditions
- Expands sulphite-reducing pathobiont Bilophila wadsworthia

Milk-derived saturated fat:
- Promotes taurine conjugation of bile acids, increasing organic sulphur for B. wadsworthia

Th1 immune response:
- High-fat diet increases colitis incidence in genetically susceptible IL10-/- mice

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13
Q

How can microbial effectors exert anti-inflammatory effects? (2)

A
  • Certain bacterial gene products drive protective inflammation in the intestine
  • Crucial for rebalancing homeostasis in inflammatory diseases and malignancies
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14
Q

How does Lactobacillus paracasei prtP-encoded lactocepin affect inflammation? (2)

A
  • Lactocepin degrades IP-10, reducing lymphocyte recruitment
  • Significantly attenuates inflammation in an ileitis model after intraperitoneal injection
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15
Q

What is the genetic aspect of colorectal cancer (CRC)? (2)

A
  • CRC is primarily a genetic disease
  • Most cases occur sporadically without a known genetic predisposition
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16
Q

How does microbial disturbance contribute to colorectal cancer (CRC)? (5)

A
  • Impairment of epithelial barrier function
  • Imbalance in epithelial self-renewal
  • DNA damage
  • Altered immune responses
  • Fosters colorectal tumour initiation and progression
17
Q

How does Escherichia coli contribute to colorectal cancer (CRC) via microbial-induced DNA damage? (3)

A
  • E. coli (group B2) produces colibactin, a genotoxin found in 30-50% of human faecal isolates
  • Precolibactin is cleaved inside host cells, causing DNA damage through cell-cycle arrest, alkylation, and double-strand breaks
  • Precancerous lesions promote colonization and expansion of pks+ E. coli strains
18
Q

How does Helicobacter hepaticus contribute to colorectal cancer (CRC)? (3)

A
  • H. hepaticus produces CDT (cytolethal distending toxin), with CdtB as the active domain
  • Induces hepatocyte proliferation, overproduction of antiapoptotic proteins, and genomic instability
  • Upregulates NF-kB pathway and downregulates IL-10, leading to colitis and colon carcinoma development
19
Q

How do microbial-induced ROS and proliferation contribute to colorectal cancer (CRC)? (4)

A

Enterotoxigenic Bacteroides fragilis:

  • Increases reactive oxygen species (ROS) and DNA damage
  • Weakens tight junctions

Fusobacterium nucleatum:

  • Elevated in colon biopsies compared to normal mucosa
  • Adhesin FadA promotes attachment, cancer cell invasion, and proliferation
20
Q

How do chemokine networks link the gut microbiome to colorectal cancer (CRC)? (4)

A

Fusobacterium nucleatum:

  • Inhibits T cells and NK cells by binding T cell immunoreceptor (TLX/PPRR ligands)

Gut microbiota:

  • Trigger chemokine production by crossing a dysfunctional epithelial barrier
  • Recruit immune cells to the lamina propria, promoting pro-inflammatory cytokine secretion
  • Increase T-cell infiltration into tumors, improving outcomes
21
Q

How does microbiota composition link T-cell-recruiting chemokines to colorectal cancer (CRC)?

A
  • T-cell-infiltrated tumors are enriched in Lachnospiraceae, Ruminococcaceae, and Bacteroidaceae, associated with T-cell-attracting factors
  • Bacteroides, Proteobacteria, and Desulfovibrio correlate with most T-cell-recruiting chemokines and higher intratumoral T-cell densities

BIOL3076 - Microbiomes and Health (17 decks)

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