A decrease in anaerobic bacteria promotes Candida glabrata overgrowth while β-glucan treatment restores the gut...

Area of Science:

• Microbiology
• Immunology
• Gastroenterology

Background:

• Intestinal microbiota is vital for gut homeostasis.
• Dysbiosis, including yeast overgrowth (e.g., Candida glabrata), is implicated in inflammatory bowel disease (IBD).
• Dextran sulfate sodium (DSS)-induced colitis models fungal dysbiosis and exacerbates inflammation.

Purpose of the Study:

• Investigate C. glabrata's impact on gut microbiota diversity during DSS-induced colitis.
• Determine the effects of soluble beta-glucans on C. glabrata-host interactions.
• Evaluate beta-glucan's therapeutic potential in colitis.

Main Methods:

• Induced acute colitis in mice using DSS and C. glabrata.
• Administered purified soluble beta-glucans orally to mice.
• Assessed C. glabrata colonization and gut microbiota composition (using culture methods) in stool samples.
• Measured inflammatory markers (e.g., IL-1β, IL-10) and gene expression (PPARγ).

Main Results:

• Colitis induced by DSS altered microbial balance, increasing E. coli and E. faecalis while decreasing L. johnsonii and B. thetaiotaomicron.
• C. glabrata overgrowth exacerbated the reduction in L. johnsonii.
• Beta-glucan treatment reduced aerobic bacteria, decreased IL-1β, and increased L. johnsonii and B. thetaiotaomicron.
• Beta-glucan administration enhanced IL-10 production via PPARγ, leading to colitis attenuation and C. glabrata clearance.

Conclusions:

• Colonic inflammation disrupts microbial equilibrium.
• Beta-glucan treatment promotes beneficial anaerobic bacteria, reduces inflammation, and clears C. glabrata.
• Beta-glucans show therapeutic promise for managing colitis and associated fungal dysbiosis.