Bifidobacterium stercoris KC84 attenuates IBS-D-like symptoms via modulation of serotonin-related pathways and dendritic cell-mediated IFN-β induction

  • Curr Res Microb Sci. 2026 May 10:10:100603. doi: 10.1016/j.crmicr.2026.100603.
Seokcheon Song  1  2 ,  Myeonghwan Han  2 ,  Kwanwoo Moon  2 ,  Haeseong Lee  2 ,  Sungchan Ha  3 ,  Juseok Seo  4 ,  Seungki Lee  4 ,  Soyong Jang  4 ,  Sang Kyun Lim  2 ,  Nayoung Kim  5 ,  GwangPyo Ko  1  2  6  7
Affiliations
  • 1. Department of Environmental Health Sciences, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea.
  • 2. KoBioLabs, Inc., Seoul, Republic of Korea.
  • 3. Department of Health Science and Technology, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, South Korea.
  • 4. R&D Division, Celltrion, Inc., Incheon, Republic of Korea.
  • 5. Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea.
  • 6. Bio-MAX/N-Bio, Seoul National University, Seoul, Republic of Korea.
  • 7. Center for Human and Environmental Microbiome, Seoul National University, Seoul, Republic of Korea.
PMID: 42199361 DOI: 10.1016/j.crmicr.2026.100603
Abstract

Irritable bowel syndrome with diarrhea (IBS-D) is a prevalent disorder that significantly impairs quality of life, yet therapeutic advances remain limited. Serotonin dysregulation, primarily driven by enterochromaffin cells in the intestinal epithelium, is central to IBS-D pathogenesis. We hypothesized that targeted modulation of enterochromaffin cell activity through microbiome-based interventions could provide a novel treatment approach. Here, we screened 128 Bifidobacterium isolates and identified B. stercoris KC84 as a promising candidate. KC84 alleviated IBS-D-like symptoms in both chemically and stress-induced models, accompanied by changes in serotonin-related markers. Transcriptomic analysis revealed activation of type I interferon (IFN)-associated pathways, consistent with ex vivo evidence of KC84-induced IFN-β secretion, predominantly from CD11b- dendritic cells. Furthermore, IFN-β treatment attenuated contractile activity in colonic smooth muscle cells. Collectively, these findings suggest that KC84 mitigates IBS-D-like symptoms, potentially through modulation of serotonin-related pathways and activation of a KC84-IFN-β-smooth muscle regulatory axis, supporting KC84 as a mechanism-guided probiotic candidate for IBS-D therapy.

Keywords
Bifidobacterium stercoris; Host microbe interaction; Interferon-β; Irritable bowel syndrome with diarrhea.
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