Long-term capsaicin intake and gut inflammation: microbial alterations, metabolic mechanisms, and intervention effects.

Long-term capsaicin intake induced gut dysbiosis characterized by an increase in Klebsiella and a decrease in Lactobacillus.

• The microbial alterations were identified through integration of a human cohort study and colonic simulation fermentation.
• The changes in Klebsiella and Lactobacillus abundance correlated significantly with gut inflammation.
• The dysbiosis was also associated with dysregulation of key metabolites including bile acids, short-chain fatty acids derivatives, and steroids.

Capsaicin metabolites including dihydrocapsaicin, ferulic acid, and veratric acid were identified in the gut.

• These metabolites were identified through the integrated human cohort and colonic simulation fermentation approach.
• The identification of these metabolites helped characterize the metabolic fate of capsaicin in the gut environment.

Escherichia and Klebsiella were identified as predominant capsaicin-utilizing gut microbes.

• Capsaicin-utilizing gut microbes were enriched and identified through experimental methods.
• Escherichia and Klebsiella were the predominant genera capable of metabolizing capsaicin among the identified microbes.

A vanillate decarboxylase homologous protein potentially involved in capsaicin metabolism was identified in Escherichia coli, Klebsiella aerogenes, and Enterococcus faecalis.

• Identification was achieved through genomic homology analysis, machine learning prediction, and molecular docking simulations.
• Expression of the vanillate decarboxylase homologous protein was positively correlated with capsaicin metabolic efficiency.
• The protein was identified across multiple strains including Escherichia coli, Klebsiella aerogenes, and Enterococcus faecalis.

Lactobacillus plantarum and Enterococcus faecalis significantly alleviated capsaicin-induced gut inflammation and repaired intestinal barrier function by directly degrading capsaicin.

• These effects were demonstrated in both cell models and human microbiota-associated animals.
• The mechanism of action involved direct degradation of capsaicin by these bacterial strains.
• Both alleviation of gut inflammation and repair of intestinal barrier function were observed outcomes of the probiotic intervention.

Long-term capsaicin intake altered gut microbiota and its metabolites to induce inflammation.

• The study integrated human cohort data with colonic simulation fermentation to characterize this mechanism.
• The research provides a foundation for managing gut health of individuals with chili habit.
• Dysregulation of key metabolites including bile acids, short-chain fatty acids derivatives, and steroids was part of the inflammatory mechanism.