Cure8 research brief
People with Crohn’s disease can have ongoing symptoms even when inflammation appears quiescent.
This study identifies mucosal gene-expression patterns and fecal microbiome signatures—including sulfur-producing microbes—that are associated with persistent symptoms, pointing to non-inflammatory mechanisms that may contribute to symptom persistence.
Researchers, gastroenterologists/clinicians, microbiome scientists, and adult IBD patients interested in causes of persistent symptoms despite quiescent disease.
This is a cross-sectional, multi-omic analysis integrating biopsy transcriptomics and fecal metagenomics from ileal and rectosigmoid sites. The ileum in symptomatic quiescent patients showed reduced expression of genes tied to immune surveillance; the rectosigmoid demonstrated reduced chemokine-related and increased ribosomal gene expression.
The study also found associations between previously reported sulfidogenic organisms and mucosal genes involved in mitochondrial metabolism, epithelial homeostasis, and neurosensory signaling. Multivariate analyses noted links between oral-associated taxa and mucosal genes related to B-cell receptor signaling and RNA processing.
The authors propose a model where altered immune regulation, microbial sulfur metabolism, and epithelial/metabolic stress pathways may underlie persistent symptoms despite quiescent inflammation. They note that mechanistic validation is still needed.
Cross-sectional multi-omic associations do not establish causality. The paper calls for mechanistic validation; results are exploratory and meant to generate hypotheses for future studies.
Review the original publication for the complete reporting, methods, and context.
This Cure8 brief is based on source text from the linked article. Cure8 is informational only and is not a substitute for professional medical advice, diagnosis, or treatment.
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