Evidence map›Paper›PMID 30099750›Full record

ReviewClinical and experimental immunology2019

Pathogen infections and primary biliary cholangitis.

A Tanaka, P S C Leung, M E Gershwin

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  7. Review
  8. Article
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  15. The gut-liver axis in hepatobiliary diseases.Inflammation and regeneration · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. [Bioinformatics analysis of primary biliary cholangitis key genes and molecular mechanisms].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
    Article
  20. Review
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

3 authors at 2 institutions in 2 countries.

A TanakaDepartment of Medicine, Teikyo University School of Medicine, Tokyo, Japan.
P S C LeungDivision of Rheumatology Allergy and Clinical Immunology, University of California School of Medicine, Davis, CA, USA.
M E GershwinDivision of Rheumatology Allergy and Clinical Immunology, University of California School of Medicine, Davis, CA, USA.
University of California, Davis · USTeikyo University · JP

Funding

XENOBIOTICS AND PRIMARY BILIARY CIRRHOSISR01DK067003 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI GERSHWIN, MERRILL E · 2003 to 2017
$4.4M
MECHANISMS AND PATHOGENESIS OF PRIMARY BILIARY CIRRHOSISR37DK039588 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI GERSHWIN, MERRILL E · 2001 to 2010
$3.5M
MECHANISMS AND PATHOGENESIS OF PRIMARY BILIARY CIRRHOSISR01DK039588 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI GERSHWIN, MERRILL E · 1988 to 2015
$2.0M
NIDDK NIH HHS R01 DK039588NIDDK NIH HHS R01 DK067003NIDDK NIH HHS R37 DK039588
6 · The paper itself

Abstract

Primary biliary cholangitis (PBC) is a multi-factorial disease caused by the interaction of both genetic predisposition and environmental triggers. Bacterial infection has been investigated most intensively, both epidemiologically and experimentally, as a prime environmental aetiology in PBC. The association of recurrent history of urinary tract infection (UTI) with PBC has been frequently confirmed by several large-scale, case-control studies, despite variation in geographic area or case-finding methods. Escherichia coli is a predominant pathogen in most cases with UTI. Animal studies and molecular mimicry analysis between the human and E. coli E2 subunit of the 2-oxo-acid dehydrogenase complexes demonstrated that E. coli infection is a key factor in breaking immunological tolerance against the mitochondria, resulting in the production of anti-mitochondrial autoantibodies (AMA), the disease-specific autoantibodies of PBC. Novosphingobium aromaticivorans, a ubiquitous xenobiotic-metabolizing bacterium, is another candidate which may be involved in the aetiology of PBC. Meanwhile, improved environmental hygiene and increased prevalence of PBC, especially in males, may argue against the aetiological role of bacterial infection in PBC. Multiple mechanisms can result in the loss of tolerance to mitochondrial autoantigens in PBC; nonetheless, bacterial infection is probably one of the dominant pathways, especially in female patients. Notably, there is a rising prevalence of male patients with PBC. With increasing exposure to environmental xenobiotics in both genders, studies directed towards identifying the environmental culprit with systematically designed case-control studies are much needed to further determine the environmental factors and role of bacterial infections in PBC.

Indexed as

Autoimmunity3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)AlphaproteobacteriaAnimalsAutoantibodiesBacterial InfectionsFemaleGene-Environment InteractionHumansImmune ToleranceLiver Cirrhosis, BiliaryMaleMitochondriaMolecular MimicryUrinary Tract Infections3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)Autoantibodiesanti-mitochondrial autoantibodiesEscherichia colimolecular mimicryNovosphingobium aromaticivoranspyruvate dehydrogenase E2 subuniturinary tract infection

Identifiers

PMID30099750
PMCPMC6300644
OpenAlexW2885219957

What OpenQuestion holds

Textmetadata
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.