Cited by 131Celiac Disease Research and ManagementProbiotics and Fermented FoodsGut microbiota and health

Bifidobacteria inhibit the inflammatory response induced by gliadins in intestinal epithelial cells via modifications of toxic peptide generation during digestion

Laparra, J.M., Sanz, Y.·2010·Journal of Cellular Biochemistry

Abstract

Celiac disease (CD) is a chronic enteropathy triggered by intake of gliadin, the toxic component of gluten. This study aims at evaluating the capacity of different Bifidobacterium strains to counteract the inflammatory effects of gliadin‐derived peptides in intestinal epithelial (Caco‐2) cells. A commercial extract of several gliadin (Gld) types (α, β, γ, ϖ) was subjected to in vitro gastrointestinal digestion (pepsin at pH 3, pancreatin‐bile at pH 6), inoculated or not with cell suspensions (10 8 colony forming units/ml) of either B. animalis IATA‐A2, B. longum IATA‐ES1, or B. bifidum IATA‐ES2, in a bicameral system. The generated gliadin‐derived peptides were identified by reverse phase‐HPLC–ESI‐MS/MS. Caco‐2 cell cultures were exposed to the different gliadin peptide digestions (0.25 mg protein/ml), and the mRNA expression of nuclear factor kappa‐B (NF‐κB), tumor necrosis factor α (TNF‐α), and chemokine CXCR3 receptor were analyzed by semi‐quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) in stimulated cells. The production of the pro‐inflammatory markers NF‐κB p50, TNF‐α, and IL‐1β (interleukine 1β) by Caco‐2 cells was also determined by ELISA. The peptides from gliadin digestions inoculated with bifidobacteria did not exhibit the toxic amino acid sequences identified in those noninoculated (α/β‐Gld [158–164] and α/β‐Gld [122‐141]). The RT‐PCR analysis evidenced a down‐regulation in mRNA expression of pro‐inflammatory biomarkers. Consistent with these results the production of NF‐κB, TNF‐α, and IL‐1β was reduced (18.2–22.4%, 28.0–64.8%, and abolished, respectively) in cell cultures exposed to gliadin digestions inoculated with bifidobacteria. Therefore, bifidobacteria change the gliadin‐derived peptide pattern and, thereby, attenuate their pro‐inflammatory effects on Caco‐2 cells. J. Cell. Biochem. 109: 801–807, 2010. © 2009 Wiley‐Liss, Inc.

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Crossref · 10.1002/jcb.22459

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  • Bifidobacteria protect human intestinal cells from the toxic effects of gliadin peptides by altering their structure.

    “Bifidobacteria protect human intestinal cells from the toxic effects of gliadin peptides, the inflammatory triggers of CD, by altering their structure.55”

    From The Gut Microbiome and the Brain (2014) · cites this paper as [55]

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Authors
Laparra, J. M., & Sanz, Y.
Affiliations
Consejo Superior de Investigaciones Científicas (ES)
Corresponding author
Sanz, Y.
Venue
Journal of Cellular Biochemistry
Publisher
Wiley
Published
2010-01-05
Volume
109
Issue
4
Pages
801-807
ISSN
  • 0730-2312 (ISSN-L)
  • 1097-4644
OpenAlex
W2080122099
Cited by
131
References
31
Citations by year
2026: 5 · 2025: 6 · 2024: 6 · 2023: 6 · 2022: 6 · 2021: 11 · 2020: 17 · 2019: 10 · 2018: 5 · 2017: 7 · 2016: 6 · 2015: 13 · 2014: 10 · 2013: 10 · 2012: 7
FWCI
7.56
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Cellular Biochemistry (publishedVersion)
  • PubMed (publishedVersion)
  • DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
Topics
  • Health Sciences › Medicine › Gastroenterology › Celiac Disease Research and Management
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
Keywords
Bifidobacterium, gliadin, celiac disease, intestinal inflammation, Caco-2 cells, NF-κB, TNF-α, IL-1β, CXCR3, gastrointestinal digestion, Bifidobacterium animalis, Bifidobacterium longum, Bifidobacterium bifidum, probiotics, gluten
MeSH terms
Bifidobacterium, Biological Therapy, Celiac Disease, Digestion, Epithelial Cells, Gliadin, Humans, Inflammation, Intestinal Mucosa, Peptide Fragments, Biomarkers, Caco-2 Cells

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