Evidence map›Paper›PMID 38987012›Full record

ArticleClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association2025

Transcriptomic and Metabolomic Correlates of Increased Colonic Permeability in Postinfection Irritable Bowel Syndrome.

Ana Y Caceres Lessa, Adam Edwinson, Hiroki Sato, Lu Yang, Antonio Berumen, Margaret Breen-Lyles, Anjali Byale, Michael Ryks, Ashley Keehn, Michael Camilleri and 6 more

Abstract read
In one paragraph

Article in Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Ana Y Caceres LessaDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota.
Adam EdwinsonDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota.
Hiroki SatoDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota; Division of Gastroenterology & Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Japan.
Lu YangDivision of Computational Biology, Mayo Clinic, Rochester, Minnesota.
Antonio BerumenDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota; Department of Medicine, Boston University, Boston, Massachusetts.
Margaret Breen-LylesDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota.
Anjali ByaleDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota; Department of Medicine, University of Pittsburgh Medical Center, McKeesport, Pennsylvania.
Michael RyksDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota.
Ashley KeehnDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota.
Michael CamilleriDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota.
Gianrico FarrugiaDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota.
Jun ChenDivision of Computational Biology, Mayo Clinic, Rochester, Minnesota.
Marijke DecuirMinnesota Department of Health, St. Paul, Minnesota.
Kirk SmithMinnesota Department of Health, St. Paul, Minnesota.
Surendra DasariBiomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota.
Madhusudan GroverDivision of Gastroenterology and Hepatology, Enteric Neuroscience Program, Mayo Clinic, Rochester, Minnesota. Electronic address: grover.madhusudan@mayo.edu.

Funding

PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI Nicholas F. LaRusso · 2009 to 2026
$22.2M
Microbiota based mechanisms of post-infection irritable bowel syndromeR01DK127998 · NIDDK · MAYO CLINIC ROCHESTER · PI GROVER, MADHUSUDAN · 2021 to 2025
$1.7M
"Barrier function alterations in post-infectious irritable bowel syndrome"K23DK103911 · NIDDK · MAYO CLINIC ROCHESTER · PI GROVER, MADHUSUDAN · 2015 to 2019
$804k
Mechanisms of barrier dysfunction in post-infection irritable bowel syndromeR03DK120745 · NIDDK · MAYO CLINIC ROCHESTER · PI GROVER, MADHUSUDAN · 2019 to 2020
$239k
NIDDK NIH HHS K23 DK103911NIDDK NIH HHS P30 DK084567NIDDK NIH HHS R01 DK127998NIDDK NIH HHS R03 DK120745
6 · The paper itself

Abstract

BACKGROUND &

aimsPostinfection irritable bowel syndrome (PI-IBS) is well-known epidemiologically; however, its physiological and molecular characteristics are not well studied. We aimed to determine the physiological phenotypes, colonic transcriptome, fecal microbiome, and metabolome in PI-IBS.

methodsFifty-one Rome III Campylobacter PI-IBS patients and 39 healthy volunteers (HV) were enrolled. Participants completed questionnaires, in vivo intestinal permeability, gastrointestinal transit, and rectal sensation. Fecal samples were collected for shotgun metagenomics, untargeted metabolomics, and sigmoid colonic biopsies for bulk RNAseq. Differential gene expression, differences in microbiota composition, and metabolite abundance were determined. Gene and metabolite clusters were identified via weighted gene correlation network analysis and correlations with clinical and physiological parameters determined.

resultsPI-IBS (59% female; 46 ± 2 years) and HV (64% female; 42 ± 2 years) demographics were comparable. Mean IBS-symptom severity score was 227; 94% were nonconstipation. Two- to 24-hour lactulose excretion was increased in PI-IBS, suggesting increased colonic permeability (4.4 ± 0.5 mg vs 2.6 ± 0.3 mg; P = .01). Colonic transit and sensory thresholds were similar between the 2 groups. Overall, expression of 2036 mucosal genes and 223 fecal metabolites were different, with changes more prominent in females. Fecal N-acetylputrescine was increased in PI-IBS and associated with colonic permeability, worse diarrhea, and negatively correlated with abundance of Collinsella aerofaciens. Histamine and N-acetylhistamine positively associated with 2- to 24-hour lactulose excretion. Eight weighted gene coexpression modules significantly correlated with phenotypes (sex, stool frequency, colonic permeability, transit).

conclusionsCampylobacter PI-IBS patients demonstrate higher colonic permeability, which associated with changes in polyamine and histamine metabolites. Female patients demonstrated greater molecular changes.

Indexed as

ColonIrritable Bowel SyndromeMetabolomeTranscriptomeAdultFecesFemaleGastrointestinal MicrobiomeHumansMaleMetabolomicsMiddle AgedPermeabilityBarrier FunctionDisorders of Gut-Brain InteractionsGastroenteritisHistamineMicrobiotaPolyamines

Identifiers

PMID38987012
PMCPMC11707044

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.