Evidence map›Paper›PMID 36569849›Full record

ReviewFrontiers in immunology2022

Bile acids as inflammatory mediators and modulators of intestinal permeability.

Nathan Calzadilla, Shane M Comiskey, Pradeep K Dudeja, Seema Saksena, Ravinder K Gill, Waddah A Alrefai

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
10.4field-weighted citation impact, top 1% of its field
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

68 citing papers in PubMed, 94 citations in OpenAlex.

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  11. Metabolomic signatures suggest altered bile acid and energy metabolism in CRB1- retinopathies.Metabolomics : Official journal of the Metabolomic Society · 2026
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8 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Nathan CalzadillaDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, IL, United States.
Shane M ComiskeyDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, IL, United States.
Pradeep K DudejaDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, IL, United States.
Seema SaksenaDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, IL, United States.
Ravinder K GillDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, IL, United States.
Waddah A AlrefaiDivision of Gastroenterology and Hepatology, Department of Medicine, University of Illinois, Chicago, IL, United States.
University of Illinois Chicago · USJesse Brown VA Medical Center · US

Funding

Intestinal Anion Transporters: Function and RegulationR01DK054016 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEJA, PRADEEP K · 1998 to 2022
$7.0M
Transporter Trafficking Mechanisms in Infectious DiarrheaR01DK092441 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEJA, PRADEEP K · 2011 to 2020
$3.0M
Intestinal 5-HT Transporter: A novel therapeutic target for GI disordersR01DK098170 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GILL, RAVINDER K · 2014 to 2022
$3.0M
Novel Role of DRA/SLC26A3 Downregulation in Gut Dysbiosis, Inflammation and InfectionR56DK092441 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEJA, PRADEEP K · 2023 to 2023
$533k
The roles of intestinal epithelial AhR in alcohol-induced barrier dysfunction and liver injuryF30AA030222 · NIAAA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CALZADILLA, NATHAN · 2022 to 2024
$96k
BLRD VA I01 BX000152BLRD VA I01 BX002011BLRD VA I01 BX002867BLRD VA I01 BX005862BLRD VA IK6 BX005242BLRD VA IK6 BX005243NIAAA NIH HHS F30 AA030222NIDDK NIH HHS R01 DK054016NIDDK NIH HHS R01 DK092441NIDDK NIH HHS R01 DK098170NIDDK NIH HHS R56 DK092441
6 · The paper itself

Abstract

Bile acids are critical for the digestion and absorption of lipids and fat-soluble vitamins; however, evidence continues to emerge supporting additional roles for bile acids as signaling molecules. After they are synthesized from cholesterol in the liver, primary bile acids are modified into secondary bile acids by gut flora contributing to a diverse pool and making the composition of bile acids highly sensitive to alterations in gut microbiota. Disturbances in bile acid homeostasis have been observed in patients with Inflammatory Bowel Diseases (IBD). In fact, a decrease in secondary bile acids was shown to occur because of IBD-associated dysbiosis. Further, the increase in luminal bile acids due to malabsorption in Crohn's ileitis and ileal resection has been implicated in the induction of diarrhea and the exacerbation of inflammation. A causal link between bile acid signaling and intestinal inflammation has been recently suggested. With respect to potential mechanisms related to bile acids and IBD, several studies have provided strong evidence for direct effects of bile acids on intestinal permeability in porcine and rodent models as well as in humans. Interestingly, different bile acids were shown to exert distinct effects on the inflammatory response and intestinal permeability that require careful consideration. Such findings revealed a potential effect for changes in the relative abundance of different bile acids on the induction of inflammation by bile acids and the development of IBD. This review summarizes current knowledge about the roles for bile acids as inflammatory mediators and modulators of intestinal permeability mainly in the context of inflammatory bowel diseases.

Indexed as

Bile Acids and SaltsInflammatory Bowel DiseasesAnimalsHumansInflammationInflammation MediatorsPermeabilitySwineBile Acids and SaltsInflammation Mediatorsbile acid receptorsbile acidsCrohn’s diseaseintestinal epithelial tight junction proteinsulcerative

Identifiers

PMID36569849
PMCPMC9768584
OpenAlexW4311714619

What OpenQuestion holds

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LicenceCC BY
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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.