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Faecalibacterium prausnitzii Attenuates DSS-Induced Colitis by Inhibiting the Colonization and Pathogenicity
Xiaqiong Mao1, Jingjing Ma1, Chunhua Jiao1
1Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Scope:
Intestinal commensal microbiota interactions play critical roles in the inflammatory bowel disease (IBD) development. Candida albicans (CA) can aggravate intestinal inflammation; however, whether Faecalibacterium prausnitzii (FP) can antagonize CA is unknown.
Methods And Results:
CA are co-cultured with bacteria (FP and Escherichia coli (EC)), bacterial supernatant, and bacterial medium, respectively. Then, the CA hyphae-specific genes' expression and CA cells' morphology are investigated. The Nod-like receptor pyrin-containing protein 6 (NLRP6) inflammasome, inflammatory cytokines, and antimicrobial peptides (AMPs) production are evaluated in intestinal epithelial cells pre-treated with bacteria, bacterial med, and bacterial supernatant and exposed without or with CA. Both bacteria significantly prohibit CA numbers, while only FP and FP supernatant prohibit the transformation and virulence factors (extracellular phospholipase, secreted aspartyl proteinase, and hemolysin) secretion of CA in a co-culture system compared with media controls. Further, FP and FP supernatant promote the production of the NLRP6 inflammasome, interleukin (IL)-1β, IL-18, and antibacterial peptides (β-defensin (BD)-2 and BD-3) and inhibit in vitro and in vivo CA growth and pathogenicity, and alleviate DSS-colitis in mice, while EC do not show the similar effect.
Conclusion:
FP improve intestinal inflammation by inhibiting CA reproduction, colonization, and pathogenicity and inducing AMP secretion in the gut. This study uncovers new relationships between intestinal microbes and fungi in IBD patients.
Insights
Faecalibacterium prausnitzii (FP) antagonizes Candida albicans (CA) by inhibiting its growth and virulence. FP also boosts antimicrobial peptide production, improving gut inflammation and potentially benefiting inflammatory bowel disease (IBD) patients.
Area of Science:
- Microbiome research
- Fungal-bacterial interactions
- Inflammatory Bowel Disease (IBD) pathogenesis
Background:
- Intestinal commensal microbiota are crucial in IBD development.
- Candida albicans (CA) can exacerbate intestinal inflammation.
- The antagonistic potential of Faecalibacterium prausnitzii (FP) against CA is unexplored.
Purpose of the Study:
- To investigate the interaction between Faecalibacterium prausnitzii (FP) and Candida albicans (CA).
- To determine if FP can antagonize CA-induced intestinal inflammation.
- To elucidate the mechanisms underlying FP's effect on CA.
Main Methods:
- Co-culture of CA with FP and Escherichia coli (EC).
- Analysis of CA gene expression, morphology, and virulence factors.
- Evaluation of NLRP6 inflammasome, cytokines, and antimicrobial peptides (AMPs) in intestinal epithelial cells.
- Assessment of FP's efficacy in a DSS-colitis mouse model.
Main Results:
- FP and FP supernatant significantly inhibited CA proliferation and virulence factor secretion.
- FP promoted NLRP6 inflammasome, IL-1β, IL-18, and AMPs (BD-2, BD-3) production.
- FP alleviated DSS-colitis in mice, while EC showed no similar effect.
- EC did not inhibit CA transformation or virulence.
Conclusions:
- FP antagonizes CA by inhibiting its reproduction, colonization, and pathogenicity.
- FP enhances intestinal health by inducing AMP secretion.
- This study reveals novel microbe-fungi interactions relevant to IBD.
