The Effect of Cucumaria frondosa Tentacles Hydrolysates on Dextran Sulfate Sodium-Induced Colitis: Integrated Metagenomics and Metabolomics Analysis

TL;DR

This study shows that Cucumaria frondosa tentacles hydrolysates reduce colitis symptoms in mice by modulating gut bacteria and inflammation.

Contribution

The study introduces a novel nutraceutical candidate for colitis treatment through integrated multi-omics analysis.

Findings

CFTHs reduced colonic inflammation and pro-inflammatory cytokines in a DSS-induced colitis model.

Metagenomic analysis showed increased Bacteroidetes and reduced Proteobacteria in CFTHs-treated mice.

Metabolomic profiling identified anti-inflammatory metabolites linked to CFTHs' therapeutic effects.

Abstract

Inflammatory bowel disease continues to pose substantial therapeutic challenges in modern gastroenterology. This study systematically evaluated the anti-colitis efficacy of Cucumaria frondosa tentacles hydrolysates (CFTHs) using a dextran sulfate sodium (DSS)-induced murine colitis model. Characterized by enhanced stability and solubility with molecular weights below 1000 Da, administration of CFTHs demonstrated a significant mitigation in colitis pathology. Therapeutic outcomes included an improved splenic index, attenuated colonic mucosal damage, and substantial decreases in serum pro-inflammatory cytokines. Relative to the DSS group, the MPO value in the CFTHs-H group decreased by 27.6%, and the IL-6 value exhibited a reduction of 33%. Metagenomic profiling revealed that CFTHs mediated gut microbiota modulation, particularly the enrichment of beneficial Bacteroidetes and suppression of pro-inflammatory Proteobacteria. Metabolomic analysis identified elevated colonic concentrations of anti-inflammatory metabolites such as gamma-linolenic acid and prostaglandin I2, suggesting a microbiome–metabolome crosstalk in the therapeutic mechanism. These multi-omics findings in a murine model suggest that CFTHs may represent a promising candidate for future studies as a nutraceutical intervention for inflammatory bowel disorder. This intervention may operate through mechanisms that include simultaneous immunomodulation, microbiota restoration, and metabolic reprogramming.

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