FP - Gut Microbiome, metabolism and pathogens Flashcards
What are indirect mechanisms of microbiota-conferred resistance? (3)
- Mucus Barrier Function: Microbiota stimulates host fucosylation, promoting mucus barrier integrity.
- Oxygen Limitation: Clostridia produce butyrate, promoting aerobic respiration in intestinal epithelial cells, reducing oxygen levels and limiting pathogen growth.
- Immune Responses: Microbial MAMPs stimulate TLRs in intestinal epithelial cells and Paneth cells, initiating immune responses that inhibit pathogens.
What are direct mechanisms of microbiota-conferred resistance? (3)
- Nutrient or Space Competition: Microbiota outcompetes pathogens for resources.
- Active Antagonism: Microbes secrete molecules like bacteriocins to kill pathogens.
- Inhibitory Metabolites: Production of compounds (e.g., secondary bile acids) inhibits pathogen growth and virulence.
Why is C. difficile considered an urgent threat by the CDC? (2)
- Severe Diarrhea: Causes debilitating diarrhea, particularly in healthcare settings.
- Antibiotic-Triggered Growth: Antibiotic use disrupts the gut microbiome, reducing colonization resistance and allowing C. difficile to overgrow.
How does the gut microbiome prevent C. difficile colonization in healthy individuals? (2)
- Diverse Microbiome: Balanced microbiota limits C. difficile growth.
- Pathogen Competition: Resident bacteria compete for resources and secrete antimicrobial compounds.
How does antibiotic treatment increase the risk of C. difficile infection? (2)
- Disrupted Microbiota: Reduced diversity weakens colonization resistance.
- Altered Environment: Changes in gut composition allow C. difficile to thrive.
How does Fecal Microbiota Transplant (FMT) help treat C. difficile infections? (2)
- Reintroduction of Healthy Microbiota: Restores microbial diversity.
- Restored Colonization Resistance: Reduces risk of C. difficile overgrowth and recurrence.
What are the steps of the FMT process? (4)
- Stool Collection: Obtained from a healthy donor.
- Processing: Stool is prepared into a solution with healthy bacteria.
- Delivery: Administered via colonoscopy, enema, or capsule.
- Recolonization: Healthy bacteria restore a balanced gut microbiome.
What did experiments with germ-free and microbiota-colonized mice show about microbiota and obesity? (4)
- Germ-Free Mice: Lean phenotype.
- Lean Microbiome: Maintains a lean phenotype.
- Obese Microbiome: Causes obesity.
- Obese Microbiome + Christensenellaceae: Restores lean phenotype, suggesting Christensenellaceae supports weight regulation.
How does the gut microbiota influence metabolic health? (3)
- Appetite Regulation: Microbiota modulates GLP-1 secretion to regulate appetite.
- Epithelial Barrier Strength: Akkermansia muciniphila improves intestinal tight junctions and glucose homeostasis.
- SCFAs and Metabolism: SCFAs inhibit hepatic fatty acid synthesis and promote fat oxidation.
How does the gut microbiota influence bile acid metabolism and lipid absorption? (2)
- Primary to Secondary Conversion: Microbiota metabolizes primary bile acids into secondary bile acids, altering the bile acid pool.
- Effect on Fatty Acid Absorption: Changes in the bile acid pool influence the efficiency of dietary fatty acid absorption.
How does the gut microbiota modulate fatty acid (FA) absorption? (2)
- Bile Acid Pool Modification: Alters the composition and concentration of bile acids in the gut lumen.
- Transporter Regulation: Modulates the expression of transporters in enterocytes that facilitate micelle absorption.
What bacterial enzymes affect bile acid function? (3)
- Bile Salt Hydrolases: Deconjugate bile acids, reducing micelle formation.
- 7α-Dehydroxylases: Convert primary to secondary bile acids, altering lipid interactions.
- Oxidases/Epimerases: Modify bile acid structure, influencing function.
