Evidence map›Paper›PMID 33917155›Full record

ArticleNutrients2021

Probiotics Supplements Reduce ER Stress and Gut Inflammation Associated with Gliadin Intake in a Mouse Model of Gluten Sensitivity.

Eleonora Ferrari, Romina Monzani, Valentina Saverio, Mara Gagliardi, Elżbieta Pańczyszyn, Valeria Raia, Valeria Rachela Villella, Gianni Bona, Marco Pane, Angela Amoruso and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  12. Frontiers in neuroscience · 2022
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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

11 authors at 3 institutions in 1 country.

Eleonora FerrariDepartment of Health Science, University of Piemonte Orientale, 28100 Novara, Italy.
Romina MonzaniDepartment of Health Science, University of Piemonte Orientale, 28100 Novara, Italy.
Valentina SaverioDepartment of Health Science, University of Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0002-1770-2661
Mara GagliardiDepartment of Health Science, University of Piemonte Orientale, 28100 Novara, Italy.
Elżbieta PańczyszynDepartment of Health Science, University of Piemonte Orientale, 28100 Novara, Italy.
Valeria RaiaRegional Cystic Fibrosis Center, Pediatric Unit, Department of Translational Medical Sciences, Federico II University Naples, 80134 Naples, Italy.
Valeria Rachela VillellaEuropean Institute for Research in Cystic Fibrosis (IERFC-Onlus), San Raffaele Scientific Institute, 20132 Milan, Italy.ORCID 0000-0003-4858-4853
Gianni BonaDivision of Pediatrics, Department of Health Science, University of Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0003-0611-7341
Marco PaneProbiotical Research Srl, 28100 Novara, Italy.
Angela AmorusoProbiotical Research Srl, 28100 Novara, Italy.
Marco CorazzariDepartment of Health Science, University of Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0002-6246-5968
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITCystic Fibrosis Research Foundation · ITProbiotical (Italy) · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to gluten, a protein present in wheat rye and barley, is the major inducer for human Celiac Disease (CD), a chronic autoimmune enteropathy. CD occurs in about 1% worldwide population, in genetically predisposed individuals bearing human leukocyte antigen (HLA) DQ2/DQ8. Gut epithelial cell stress and the innate immune activation are responsible for the breaking oral tolerance to gliadin, a gluten component. To date, the only treatment available for CD is a long-term gluten-free diet. Several studies have shown that an altered composition of the intestinal microbiota (dysbiosis) could play a key role in the pathogenesis of CD through the modulation of intestinal permeability and the regulation of the immune system. Here, we show that gliadin induces a chronic endoplasmic reticulum (ER) stress condition in the small intestine of a gluten-sensitive mouse model and that the coadministration of probiotics efficiently attenuates both the unfolded protein response (UPR) and gut inflammation. Moreover, the composition of probiotics formulations might differ in their activity at molecular level, especially toward the three axes of the UPR. Therefore, probiotics administration might potentially represent a new valuable strategy to treat gluten-sensitive patients, such as those affected by CD.

Indexed as

Dietary SupplementsEndoplasmic Reticulum StressAnimalsAnti-Inflammatory AgentsCaco-2 CellsCystic Fibrosis Transmembrane Conductance RegulatorDisease Models, AnimalFood IntoleranceGastrointestinal TractGliadinGlutensGTP-Binding ProteinsHumansInflammationMiceMice, Inbred BALB CAnti-Inflammatory AgentsCystic Fibrosis Transmembrane Conductance RegulatorGliadinGlutensGTP-Binding ProteinsProtein Glutamine gamma Glutamyltransferase 2TransglutaminasesCDCFTRprobioticsTG2UPR

Identifiers

PMID33917155
PMCPMC8067866
OpenAlexW3142849451

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.