Impact of terminal ileal microbiota dysbiosis and tryptophan metabolism alterations on mental disorders in patients with Crohn's diseaseOriginal paper
What was studied?
This study asked how terminal ileal microbiota and tryptophan metabolism relate to anxiety and depression in Crohn's disease. It focused on the mucosa at the ileum, a common Crohn's site, rather than feces. Mucosa was collected during surgery. Microbiota were profiled by 16S rRNA sequencing and tryptophan catabolites quantified by LC-MS/MS. Mental disorder status was set by PHQ-9 and GAD-7 questionnaires, then correlated with microbes and metabolites.
Who was studied?
The cohort was 52 Crohn's disease patients (ileal or ileocolic type) and 11 colorectal cancer patients as controls, treated at Shanghai Tenth People's Hospital, China. Crohn's patients averaged about 40 years old. Microbiota analysis covered 37 Crohn's patients (24 with mental disorders, 13 with normal behavior). Tryptophan metabolomics covered 28 patients (16 with mental disorders). All had ileocecal resection. Prior psychiatric illness, recent antibiotics, and probiotics were exclusion criteria.
What were the most important findings?
Crohn's patients with mental disorders showed significantly lower Chao1 and Faith_pd diversity in the ileal mucosa. Prevotella was enriched, while Akkermansia and Faecalibacterium were significantly depleted. Comorbid mental disorders were common: 63.5% of Crohn's patients versus 18.2% of controls. PHQ-9 correlated with disease activity and sleep quality. Tryptophan catabolites picolinic acid, kynurenic acid, nicotinic acid and indole-3-carbaldehyde were elevated. Picolinic acid correlated with anxiety scores and with Prevotella abundance.
What are the greatest implications of this study?
The results suggest ileal mucosal dysbiosis and altered tryptophan metabolism accompany anxiety and depression in Crohn's disease. Depleted Akkermansia and Faecalibacterium and enriched Prevotella may weaken anti-inflammatory and psychobiotic capacity. Microbes and tryptophan pathways emerge as candidate targets for reducing psychological burden. The cross-sectional design cannot prove causation. Cancer controls, questionnaire-based diagnosis, and small samples limit the findings, so healthy controls and larger cohorts are needed.