Evidence map›Paper›PMID 32423041›Full record

ArticleNutrients2020

A Two-Sample Mendelian Randomization Analysis Investigates Associations Between Gut Microbiota and Celiac Disease.

Iraia García-Santisteban, Ariadna Cilleros-Portet, Elisabet Moyua-Ormazabal, Alexander Kurilshikov, Alexandra Zhernakova, Koldo Garcia-Etxebarria, Nora Fernandez-Jimenez, Jose Ramon Bilbao

Open access · goldAbstract readEvaluation Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Iraia García-SantistebanDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country (UPV/EHU) and Biocruces-Bizkaia Health Research Institute, 48940 Leioa, Spain.
Ariadna Cilleros-PortetDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country (UPV/EHU) and Biocruces-Bizkaia Health Research Institute, 48940 Leioa, Spain.
Elisabet Moyua-OrmazabalDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country (UPV/EHU) and Biocruces-Bizkaia Health Research Institute, 48940 Leioa, Spain.
Alexander KurilshikovDepartment of Genetics, University of Groningen and University Medical Center Groningen, 9713 GZ Groningen, The Netherlands.
Alexandra ZhernakovaDepartment of Genetics, University of Groningen and University Medical Center Groningen, 9713 GZ Groningen, The Netherlands.
Koldo Garcia-EtxebarriaBiodonostia, Gastrointestinal genetics group, 20014 San Sebastian, Spain.
Nora Fernandez-JimenezDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country (UPV/EHU) and Biocruces-Bizkaia Health Research Institute, 48940 Leioa, Spain.
Jose Ramon BilbaoDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country (UPV/EHU) and Biocruces-Bizkaia Health Research Institute, 48940 Leioa, Spain.
University of the Basque Country · ESUniversity Medical Center Groningen · NLBiogipuzkoa Health Research Institute · ES

Funding

Osasun Saila, Eusko Jaurlaritzako GVSAN2018/111086Osasun Saila, Eusko Jaurlaritzako GVSAN2019/111085
6 · The paper itself

Abstract

Celiac disease (CeD) is a complex immune-mediated inflammatory condition triggered by the ingestion of gluten in genetically predisposed individuals. Literature suggests that alterations in gut microbiota composition and function precede the onset of CeD. Considering that microbiota is partly determined by host genetics, we speculated that the genetic makeup of CeD patients could elicit disease development through alterations in the intestinal microbiota. To evaluate potential causal relationships between gut microbiota and CeD, we performed a two-sample Mendelian randomization analysis (2SMR). Exposure data were obtained from the raw results of a previous genome-wide association study (GWAS) of gut microbiota and outcome data from summary statistics of CeD GWAS and Immunochip studies. We identified a number of putative associations between gut microbiota single nucleotide polymorphisms (SNPs) associated with CeD. Regarding bacterial composition, most of the associated SNPs were related to Firmicutes phylum, whose relative abundance has been previously reported to be altered in CeD patients. In terms of functional units, we linked a number of SNPs to several bacterial metabolic pathways that seemed to be related to CeD. Overall, this study represented the first 2SMR approach to elucidate the relationship between microbiome and CeD.

Indexed as

Celiac DiseaseGastrointestinal MicrobiomeGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single Nucleotideceliac diseasegut microbiotaMendelian randomization

Identifiers

PMID32423041
PMCPMC7284592
OpenAlexW3013549741

What OpenQuestion holds

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Registered trials

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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.