Mucosal transcriptomic and fecal microbiome signatures associated with persistent symptoms in quiescent Crohn's disease.

Authors

Kexin Guo, Jonathan Golob, Jeffrey Berinstein, Jessica Sheehan, William D Chey, Peter D R Higgins, Vincent Young, Krishna Rao, Prashant Singh, Shrinivas Bishu, Allen Lee

Published in

Inflammatory bowel diseases. Nov 05, 2026. Epub Nov 05, 2026.

Abstract

Persistent symptoms in quiescent Crohn's disease (qCD + S) lack clear mechanistic explanations. Building on prior evidence linking qCD + S to sulfidogenic microbial metabolism, this study characterizes the underlying site-specific mucosal transcriptional programs and host-microbe interactions associated with qCD + S.
We integrated paired metagenomic and transcriptomic data from a cross-sectional cohort of patients with qCD. Host-microbe interactions in the ileum and rectosigmoid colon were analyzed using differential expression, penalized regression, and sparse canonical correlation analysis.
qCD + S was associated with transcriptional differences in separate analyses of ileal and rectosigmoid samples. The ileum showed reduced expression of genes related to immune surveillance, whereas the rectosigmoid colon exhibited reduced chemokine-related and increased ribosomal gene expression. Multi-omic integration identified associations between previously identified sulfidogenic microbes and mucosal genes related to mitochondrial metabolism, epithelial homeostasis, and neurosensory signaling. Exploratory sparse canonical correlation analysis identified multivariate patterns involving oral-associated taxa and mucosal genes related to B-cell receptor signaling and RNA-processing.
Persistent symptoms in qCD are mucosal transcriptional differences and fecal microbial features. These findings suggest a model in which altered immune regulation, microbial sulfur metabolism, and downstream epithelial and metabolic stress pathways contribute to symptom persistence despite quiescent inflammation, but this model requires mechanistic validation.

PMID:
42986703
Bibliographic data and abstract were imported from PubMed on 06 Nov 2026.

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