Evidence map›Paper›PMID 29672211›Full record

ArticleGut microbes2018

Increased prevalence of pathogenic bacteria in the gut microbiota of infants at risk of developing celiac disease: The PROFICEL study.

Marta Olivares, Alfonso Benítez-Páez, Giada de Palma, Amalia Capilla, Esther Nova, Gemma Castillejo, Vicente Varea, Ascensión Marcos, José Antonio Garrote, Isabel Polanco and 6 more

Open access · goldAbstract read
In one paragraph

Article in Gut microbes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Harnessing gut microbiome enzymes:Microbiology spectrum · 2026
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  10. Variations in gut microbiota in celiac disease patients: a systematic review.Gastroenterology and hepatology from bed to bench · 2025
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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

16 authors at 7 institutions in 1 country.

Marta Olivaresa Microbial Ecology, Nutrition & Health Research Unit. Institute of Agrochemistry and Food Technology, Spanish National Research Council (IATA-CSIC) , Valencia , Spain.ORCID 0000-0002-7966-2781
Alfonso Benítez-Páeza Microbial Ecology, Nutrition & Health Research Unit. Institute of Agrochemistry and Food Technology, Spanish National Research Council (IATA-CSIC) , Valencia , Spain.
Giada de Palmaa Microbial Ecology, Nutrition & Health Research Unit. Institute of Agrochemistry and Food Technology, Spanish National Research Council (IATA-CSIC) , Valencia , Spain.
Amalia Capillab Genetics and Molecular Medicine Unit. Institute of Biomedicine of Valencia, Spanish National Research Council (IBV-CSIC) , Valencia , Spain.
Esther Novac Institute of Food Science, Technology and Nutrition, Spanish National Research Council (ICTAN-CSIC) , Madrid , Spain.
Gemma Castillejod Universitary Hospital Sant Joan of Reus, URV, IISPV , Tarragona , Spain.
Vicente Vareae Gastroenterología, Nutrición y Hepatología Pediátrica, Hospital Universitario Sant Joan de Deu, and Instituto de Gastroeneterología y Nutrición Pediátrica de Barcelona , Barcelona , Spain.
Ascensión Marcosc Institute of Food Science, Technology and Nutrition, Spanish National Research Council (ICTAN-CSIC) , Madrid , Spain.
José Antonio Garrotef Research Unit and Paediatric Service, Hospital Clínico Universitario , Valladolid , Spain.
Isabel Polancog Servicio de Gastroenterología y Nutrición Pediátrica, Hospital Universitario La Paz , Madrid , Spain.
Ester Donath Unidad de Gastroenterología, Hospital Infantil Universitario La Fe , Valencia , Spain.ORCID 0000-0002-0114-6445
Carmen Ribes-Koninckxh Unidad de Gastroenterología, Hospital Infantil Universitario La Fe , Valencia , Spain.
Carmen Calvof Research Unit and Paediatric Service, Hospital Clínico Universitario , Valladolid , Spain.
Luis Ortigosai Unidad de Gastroenterologia, Hepatología y Nutrición Pediátrica, Hospital Universitario Nuestra Señora de Candelaria , Santa Cruz de Tenerife, Canary Islands , Spain.
Francesc Palaub Genetics and Molecular Medicine Unit. Institute of Biomedicine of Valencia, Spanish National Research Council (IBV-CSIC) , Valencia , Spain.
Yolanda Sanza Microbial Ecology, Nutrition & Health Research Unit. Institute of Agrochemistry and Food Technology, Spanish National Research Council (IATA-CSIC) , Valencia , Spain.
Consejo Superior de Investigaciones Científicas · ESHospital Clínico Universitario de Valladolid · ESHospital Universitari i Politècnic La Fe · ESHospital Sant Joan de Déu Barcelona · ESHospital Universitario La Paz · ESHospital Universitario Nuestra Señora de Candelaria · ESInstitut de Recerca Biomèdica Catalunya Sud · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celiac disease (CD) is an immune-mediated enteropathy involving genetic and environmental factors, whose interaction influences disease risk. The intestinal microbiota, including viruses and bacteria, could play a role in the pathological process leading to gluten intolerance. In this study, we investigated the prevalence of pathogens in the intestinal microbiota of infants at familial risk of developing CD. We included 127 full-term newborns with at least one first-degree relative with CD. Infants were classified according to milk-feeding practice (breastfeeding or formula feeding) and HLA-DQ genotype (low, intermediate or high genetic risk). The prevalence of pathogenic bacteria and viruses was assessed in the faeces of the infants at 7 days, 1 month and 4 months of age. The prevalence of Clostridium perfringens was higher in formula-fed infants than in breast-fed over the study period, and that of C. difficile at 4 months. Among breastfed infants, a higher prevalence of enterotoxigenic E. coli (ETEC) was found in infants with the highest genetic risk compared either to those with a low or intermediate risk. Among formula-fed infants, a higher prevalence of ETEC was also found in infants with a high genetic risk compared to those of intermediate risk. Our results show that specific factors, such as formula feeding and the HLA-DQ2 genotype, previously linked to a higher risk of developing CD, influence the presence of pathogenic bacteria differently in the intestinal microbiota in early life. Further studies are warranted to establish whether these associations are related to CD onset later in life.

Indexed as

Gastrointestinal MicrobiomeGenetic Predisposition to DiseaseBacteriaCeliac DiseaseClostridiumEnterotoxigenic Escherichia coliFecesFeeding BehaviorGenotypeHLA-DQ AntigensHumansInfant, NewbornRiskSpainHLA-DQ2 antigenHLA-DQ Antigensceliac diseasegut microbiotaHLA genotypepathogenic bacteriaPCR

Identifiers

PMID29672211
PMCPMC6287676
OpenAlexW2802663596

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.