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. 2015 Jul 28;10(7):e0134050.
doi: 10.1371/journal.pone.0134050. eCollection 2015.

"V体育安卓版" Bifidobacterium longum CCM 7952 Promotes Epithelial Barrier Function and Prevents Acute DSS-Induced Colitis in Strictly Strain-Specific Manner

Dagmar Srutkova  1 , Martin Schwarzer  1 , Tomas Hudcovic  1 , Zuzana Zakostelska  2 , Vladimir Drab  3 , Alena Spanova  4 , Bohuslav Rittich  4 , Hana Kozakova  1 , Irma Schabussova  5
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Bifidobacterium longum CCM 7952 Promotes Epithelial Barrier Function and Prevents Acute DSS-Induced Colitis in Strictly Strain-Specific Manner (V体育2025版)

Dagmar Srutkova et al. PLoS One. .

Abstract

Background: Reduced microbial diversity has been associated with inflammatory bowel disease (IBD) and probiotic bacteria have been proposed for its prevention and/or treatment. Nevertheless, comparative studies of strains of the same subspecies for specific health benefits are scarce. Here we compared two Bifidobacterium longum ssp VSports手机版. longum strains for their capacity to prevent experimental colitis. .

Methods: Immunomodulatory properties of nine probiotic bifidobacteria were assessed by stimulation of murine splenocytes. The immune responses to B. longum ssp. longum CCM 7952 (Bl 7952) and CCDM 372 (Bl 372) were further characterized by stimulation of bone marrow-derived dendritic cell, HEK293/TLR2 or HEK293/NOD2 cells V体育安卓版. A mouse model of dextran sulphate sodium (DSS)-induced colitis was used to compare their beneficial effects in vivo. .

Results: The nine bifidobacteria exhibited strain-specific abilities to induce cytokine production. Bl 372 induced higher levels of both pro- and anti-inflammatory cytokines in spleen and dendritic cell cultures compared to Bl 7952. Both strains engaged TLR2 and contain ligands for NOD2 V体育ios版. In a mouse model of DSS-induced colitis, Bl 7952, but not Bl 372, reduced clinical symptoms and preserved expression of tight junction proteins. Importantly, Bl 7952 improved intestinal barrier function as demonstrated by reduced FITC-dextran levels in serum. .

Conclusions: We have shown that Bl 7952, but not Bl 372, protected mice from the development of experimental colitis VSports最新版本. Our data suggest that although some immunomodulatory properties might be widespread among the genus Bifidobacterium, others may be rare and characteristic only for a specific strain. Therefore, careful selection might be crucial in providing beneficial outcome in clinical trials with probiotics in IBD. .

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Conflict of interest statement

Competing Interests: Here the authors state that Dairy Research Institute Ltd provided support in the form of providing research material, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. Furthermore, none of the funding bodies had any role in study design, data collection and analysis, decision to publish, or preparation of the manuscript V体育平台登录. The fact that the authors' work was funded by several funding bodies and one of the authors is employed by a commercial company does not alter the authors' adherence to PLOS ONE policies on sharing data and material.

Figures

Fig 1
Fig 1. Stimulation of bone marrow-derived dendritic cells with Bl 7952 and Bl 372.
Bone marrow-derived dendritic cells (BM-DC) from naïve mice were cultured with formalin-inactivated Bl 7952 or Bl 372 (107 CFU/ml) for 18 h. Ultra-pure lipopolysaccharide from E. coli (LPS, 1 μg/ml) and Pam3CSK4 (PAM3C, 1 μg/ml) were used as positive controls. Untreated cells (M) served as negative control. (A) Expression of CD40, CD80 and CD86 was assessed by means of flow cytometry. BM-DCs were gated as MHCII+CD11c+. Numbers represent florescence units from one representative experiment out of three. (B) Cytokines in cell culture supernatants were determined by ELISA. Results are representative of three repeat experiments. Data are expressed as mean ± SEM. Significant differences between cytokine levels of experimental group to negative control (M) was calculated using One-way ANOVA and Dunnett’s multiple comparison post-hoc test (**p < 0.01, ***p < 0.001).
Fig 2
Fig 2. Activation of TLR2 and NOD2 by Bl 7952 and Bl 372.
Human embryonic kidney cells (HEK293) stably transfected with an expression vector for human TLR2 (293-hTLR2/CD14) or with NOD2 (293-hNOD2) were stimulated with formalin-inactivated Bl 7952 or Bl 372 for 20 h. Stimulation was performed at concentrations of 106, 107 or 108 CFU/ml. Cells stimulated with ultra-pure lipopolysaccharide from E. coli (LPS, 1 μg/ml) or untreated cells (M) were used as negative controls. Cells stimulated with Pam3CSK4 (PAM3C, 1 μg/ml) or muramyl dipeptide (MDP, 1 μg/ml) were used as positive controls for TLR2 or NOD2, respectively. Data are expressed as one representative experiment out of three.
Fig 3
Fig 3. Impact of Bl 7952 and Bl 372 on DSS-induced colitis.
(A) Mice were treated with Bl 7952 (n = 10), with Bl 372 (n = 8) or with PBS (n = 10) on ten consecutive days. Naïve animals (n = 5) were left untreated. Colonic inflammation was induced by the addition of 2.5% (w/v) DSS in the drinking water for 7 days. (B) Disease activity index and (C) colon length were evaluated at the end of the experiment. (D) Body weight of mice was evaluated throughout the experiment and the values are expressed as percentage of change of the initial value measured before DSS administration. Changes in colonic mucosa after DSS-treatment are shown on representative histological sections of healthy untreated mice (Naïve), mice treated with PBS (PBS/DSS), Bl 7952 (Bl 7952/DSS) or Bl 372 (Bl 372/DSS). The sections were stained by H&E (E) to address the degree of inflammation and by alcian blue (F) to show the changes in production of mucus in colonic tissue. Graphs show mean ± SEM and represent one out of two experiments. Unpaired Student’s t-test was used for comparison of experimental groups vs. control PBS/DSS group (*p < 0.05, ***p < 0.001).
Fig 4
Fig 4. Bl 7952 strain downregulated the secretion of pro-inflammatory cytokines in mesenteric lymph node cells of mice with DSS-induced colitis.
Spontaneous production of anti-inflammatory IL-10 (A) or pro-inflammatory cytokines TNF-α (B) and IFN-γ (C) were analysed by multiplex assay in supernatants of mesenteric lymph node cells incubated with media only for 48 h. Data are expressed as mean ± SEM of untreated (n = 5), PBS/DSS (n = 10), Bl 7952/DSS (n = 10) or Bl 372/DSS (n = 8) mice. Unpaired Student’s t-test was used for comparison of experimental groups vs. PBS/DSS groups (*p < 0.05).
Fig 5
Fig 5. Bl 7952 induces upregulation of zonulin-1 and occludin in colon.
Mice were treated with Bl 7952 (n = 10), with Bl 372 (n = 8) or with PBS (n = 10) on ten consecutive days or were left untreated (Naïve; n = 5). Colonic inflammation was induced by addition of 2.5% (w/v) DSS in the drinking water for 7 days. (A) Immunohistochemical detection of occludin and zonulin-1 proteins on representative paraffin-embedded sections of colon. (B) Representative western blotting of occludin and zonulin-1 proteins in the colonic mucosa. Expression of β-actin was used as internal control. (C) Evaluation of intestinal permeability by FITC-dextran. Serum levels of 4.0-kDa FITC-dextran were measured in naïve controls (n = 5), PBS/DSS-treated (n = 5) and Bl 7952/DSS-treated mice (n = 5) 5 hours after its intragastric administration. Data are express as mean ± SEM. Unpaired Student’s t-test was used for comparison of Bl 7952/DSS group vs. control PBS/DSS group (**p < 0.01).
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References

    1. Baumgart DC, Sandborn WJ. Crohn's disease. The Lancet. 2012;380(9853):1590–605. 10.1016/s0140-6736(12)60026-9 - "VSports在线直播" DOI - PubMed
    1. Boirivant M, Cossu A. Inflammatory bowel disease. Oral Dis. 2012;18(1):1–15. Epub 2011/05/14. 10.1111/j.1601-0825.2011.01811.x . - DOI - PubMed
    1. Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012;142(1):46–54 e42; quiz e30. Epub 2011/10/18. 10.1053/j.gastro.2011.10.001 . - DOI - PubMed
    1. Weinstock JV, Elliott DE. Translatability of helminth therapy in inflammatory bowel diseases. Int J Parasitol. 2013;43(3–4):245–51. Epub 2012/11/28. 10.1016/j.ijpara.2012.10.016 - V体育ios版 - DOI - PMC - PubMed
    1. Manichanh C, Borruel N, Casellas F, Guarner F. The gut microbiota in IBD. Nat Rev Gastroenterol Hepatol. 2012;9(10):599–608. Epub 2012/08/22. 10.1038/nrgastro.2012.152 . - VSports注册入口 - DOI - PubMed

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