Bifidobacterium longum CECT 7347 Modulates Immune Responses in a Gliadin-Induced Enteropathy Animal Model
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Coeliac disease (CD) is an autoimmune disorder triggered by gluten proteins (gliadin) that involves innate and adaptive immunity. In this study, we hypothesise that the administration of Bifidobacterium longum CECT 7347, previously selected for reducing gliadin immunotoxic effects in vitro, could exert protective effects in an animal model of gliadin-induced enteropathy. The effects of this bacterium were evaluated in newborn rats fed gliadin alone or sensitised with interferon (IFN)-γ and fed gliadin. Jejunal tissue sections were collected for histological, NFκB mRNA expression and cytokine production analyses. Leukocyte populations and T-cell subsets were analysed in peripheral blood samples. The possible translocation of the bacterium to different organs was determined by plate counting and the composition of the colonic microbiota was quantified by real-time PCR. Feeding gliadin alone reduced enterocyte height and peripheral CD4+ cells, but increased CD4+/Foxp3+ T and CD8+ cells, while the simultaneous administration of B. longum CECT 7347 exerted opposite effects. Animals sensitised with IFN-γ and fed gliadin showed high cellular infiltration, reduced villi width and enterocyte height. Sensitised animals also exhibited increased NFκB mRNA expression and TNF-α production in tissue sections. B. longum CECT 7347 administration increased NFκB expression and IL-10, but reduced TNF-α, production in the enteropathy model. In sensitised gliadin-fed animals, CD4+, CD4+/Foxp3+ and CD8+ T cells increased, whereas the administration of B. longum CECT 7347 reduced CD4+ and CD4+/Foxp3+ cell populations and increased CD8+ T cell populations. The bifidobacterial strain administered represented between 75-95% of the total bifidobacteria isolated from all treated groups, and translocation to organs was not detected. These findings indicate that B. longum attenuates the production of inflammatory cytokines and the CD4+ T-cell mediated immune response in an animal model of gliadin-induced enteropathy.
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Administration of Bifidobacterium longum ameliorates an animal model of gluten enteropathy.
“Administration of Bifidobacterium longum ameliorates an animal model of gluten enteropathy,58”
From The Gut Microbiome and the Brain (2014) · cites this paper as [58]
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- Authors
- Laparra, J. M., Olivares, M., Gallina, O., & Sanz, Y.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Sanz, Yolanda
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-02-10
- Volume
- 7
- Issue
- 2
- Pages
- e30744
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3277586
- OpenAlex
- W2078908888
- Cited by
- 153
- References
- 39
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 11 · 2023: 13 · 2022: 12 · 2021: 20 · 2020: 19 · 2019: 6 · 2018: 6 · 2017: 8 · 2016: 7 · 2015: 12 · 2014: 13 · 2013: 12 · 2012: 5
- FWCI
- 12.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (acceptedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministerio de Ciencia e Innovación (AGL2007-66126-C03-01/ALI, CSD2007-00063)
- 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
- celiac disease, gluten, probiotics, NF-κB, TNF-α, IL-10, Th1/Th2 balance, regulatory T cells, CD8+ T cells, intestinal inflammation, colonic microbiota, bacterial translocation, enterocyte morphology
- MeSH terms
- Animals, Animals, Newborn, Bifidobacterium, Biological Therapy, Celiac Disease, Disease Models, Animal, Female, Gliadin, Immunity, Inflammation, Mice, Inbred C57BL, CD4-Positive T-Lymphocytes, Cytokines, Mice, Rats
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