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Bifidobacteria inhibit the inflammatory response induced by gliadins in intestinal epithelial cells via modifications of toxic peptide generation during digestion
Author(s) -
Laparra J.M.,
Sanz Y.
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22459
Subject(s) - peptide , chemistry , digestion (alchemy) , inflammatory response , microbiology and biotechnology , inflammation , biochemistry , biology , immunology , chromatography
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.