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FMT from IBS-D Rats Impairs Intestinal Barrier Function and is Associated with Increased Intestinal Benzoic Acid and
Xiangyu Xie1, Weixin Yan2, Xinting Zhang1
1The First Clinical School of Guangzhou University of Chinese Medicine, Guangzhou 510405, P. R. China.
Journal of Microbiology and Biotechnology
|June 17, 2026
Summary
Fecal microbiota transplantation (FMT) from IBS-D rats induced IBS-D symptoms in recipients. Gut bacteria like Ruminococcaceae and metabolites such as benzoic acid were linked to disease progression and gut barrier dysfunction.
Area of Science:
- Gastroenterology
- Microbiology
- Immunology
Background:
- Diarrhea-predominant irritable bowel syndrome (IBS-D) has a multifactorial etiology, with gut microbiota dysbiosis increasingly recognized as a key factor.
- Understanding the specific microbial and metabolic contributions to IBS-D pathogenesis is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of gut microbiota in the progression of IBS-D.
- To elucidate the underlying mechanisms by which gut microbiota influences IBS-D pathophysiology.
- To identify specific bacterial taxa and metabolites associated with IBS-D.
Main Methods:
- Establishment of a rat model of IBS-D exhibiting visceral hypersensitivity and diarrhea.
- Fecal microbiota transplantation (FMT) from IBS-D rats to antibiotic-treated recipient rats.
- Assessment of IBS-D-like symptoms, intestinal barrier integrity (tight junction proteins), inflammation markers (TNF-α, IL-10), and gut microbiota composition (16S rRNA sequencing) and metabolomics.
Main Results:
- FMT successfully recapitulated IBS-D-like symptoms, including abdominal pain, diarrhea, and depression-like behaviors in recipient rats.
- Both IBS-D and FMT-recipient rats showed disrupted intestinal barrier integrity (reduced tight junction proteins) and low-grade inflammation (elevated DAO and TNF-α, reduced IL-10).
- An increased abundance of Ruminococcaceae and enrichment in the phenylalanine, tyrosine, and tryptophan biosynthesis pathway, particularly benzoic acid, were common features. Ruminococcus abundance correlated positively with benzoic acid levels.
Conclusions:
- Fecal microbiota transplantation effectively models key aspects of IBS-D pathophysiology, confirming the gut microbiota's central role.
- Disruption of intestinal barrier function and induction of low-grade inflammation are critical mechanisms.
- Ruminococcaceae and benzoic acid represent potential microbial and metabolic targets for understanding and treating IBS-D.
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