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Colonization of C57BL/6 Mice by a Potential Probiotic Bifidobacterium bifidum Strain under Germ-Free and Specific Pathogen-Free Conditions and during Experimental Colitis.

Grimm V, Radulovic K, Riedel CU - PLoS ONE (2015)

Bottom Line: Colonization of and persistence in the gastrointestinal tract is thus contributing to the beneficial effects of these strains.Conversely, B. bifidum S17/pMGC, i.e., a strain of human origin, adhered at significantly higher levels to human compared to murine IECs (p < 0.001).Collectively, these results suggest a selective disadvantage of B. bifidum S17/pMGC in the competition with the normal murine microbiota and an anti-inflammatory effect that requires live, metabolically active bacteria.

View Article: PubMed Central - PubMed

Affiliation: Institute of Microbiology and Biotechnology, University of Ulm, 89068, Ulm, Germany.

ABSTRACT
The effects of at least some probiotics are restricted to live, metabolically active bacteria at their site of action. Colonization of and persistence in the gastrointestinal tract is thus contributing to the beneficial effects of these strains. In the present study, colonization of an anti-inflammatory Bifidobacterium bifidum strain was studied in C57BL/6J mice under germ-free (GF) and specific pathogen-free (SPF) conditions as well as during dextran sulfate sodium (DSS)-induced colitis. B. bifidum S17/pMGC was unable to stably colonize C57BL/6J mice under SPF conditions. Mono-association of GF mice by three doses on consecutive days led to long-term, stable detection of up to 109 colony forming units (CFU) of B. bifidum S17/pMGC per g feces. This stable population was rapidly outcompeted upon transfer of mono-associated animals to SPF conditions. A B. animalis strain was isolated from the microbiota of these re-conventionalized mice. This B. animalis strain displayed significantly higher adhesion to murine CMT-93 intestinal epithelial cells (IECs) than to human Caco-2 IECs (p = 0.018). Conversely, B. bifidum S17/pMGC, i.e., a strain of human origin, adhered at significantly higher levels to human compared to murine IECs (p < 0.001). Disturbance of the gut ecology and induction of colitis by DSS-treatment did not promote colonization of the murine gastrointestinal tract (GIT) by B. bifidum S17/pMGC. Despite its poor colonization of the mouse GIT, B. bifidum S17/pMGC displayed a protective effect on DSS-induced colitis when administered as viable bacteria but not as UV-inactivated preparation. Collectively, these results suggest a selective disadvantage of B. bifidum S17/pMGC in the competition with the normal murine microbiota and an anti-inflammatory effect that requires live, metabolically active bacteria.

No MeSH data available.


Related in: MedlinePlus

UV-killed B. bifidum S17 does not protect C57BL/6J mice against DSS-induced colitis.(A) Effect of UV-killed B. bifidum S17/pMGC on DSS-induced weight loss (A) and increase in colonic weight:length ratio (B). Mice were treated with B. bifidum S17/pMGC and challenged with DSS (DSS/S17). Control mice received PBS as placebo and water with or without DSS (DSS/PBS and H2O/PBS respectively, all groups n = 5). Values are mean ± standard error of the mean. Statistical analysis was performed by one-way ANOVA with Bonferroni post-test analysis for each day (B) or at the end of the trial (C). Asterisks indicate levels of statistical significance differences for comparison to H2O/PBS group (*: p < 0.05; ***: p<0.001).
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pone.0139935.g006: UV-killed B. bifidum S17 does not protect C57BL/6J mice against DSS-induced colitis.(A) Effect of UV-killed B. bifidum S17/pMGC on DSS-induced weight loss (A) and increase in colonic weight:length ratio (B). Mice were treated with B. bifidum S17/pMGC and challenged with DSS (DSS/S17). Control mice received PBS as placebo and water with or without DSS (DSS/PBS and H2O/PBS respectively, all groups n = 5). Values are mean ± standard error of the mean. Statistical analysis was performed by one-way ANOVA with Bonferroni post-test analysis for each day (B) or at the end of the trial (C). Asterisks indicate levels of statistical significance differences for comparison to H2O/PBS group (*: p < 0.05; ***: p<0.001).

Mentions: Since stable colonization is not required for its probiotic effect, it was further investigated if administration of killed bacteria yields a similar protective effect. To this end, the DSS trial was repeated, however, mice were treated with UV-killed B. bifidum S17/pMGC. Inactivation of B. bifidum S17/pMGC completely abolished the protective affect on DSS-induced weight loss (Fig 6A). Also, the increase in colon weight:length ratio of DSS-challenged, placebo-treated animals compared to the mice receiving H2O and placebo (6.4 ± 0.9 vs. 3.9 ± 0.6 mg/mm) was not prevented by treatment with UV-killed bacteria (6.5 ± 1.0 mg/mm; Fig 6B).


Colonization of C57BL/6 Mice by a Potential Probiotic Bifidobacterium bifidum Strain under Germ-Free and Specific Pathogen-Free Conditions and during Experimental Colitis.

Grimm V, Radulovic K, Riedel CU - PLoS ONE (2015)

UV-killed B. bifidum S17 does not protect C57BL/6J mice against DSS-induced colitis.(A) Effect of UV-killed B. bifidum S17/pMGC on DSS-induced weight loss (A) and increase in colonic weight:length ratio (B). Mice were treated with B. bifidum S17/pMGC and challenged with DSS (DSS/S17). Control mice received PBS as placebo and water with or without DSS (DSS/PBS and H2O/PBS respectively, all groups n = 5). Values are mean ± standard error of the mean. Statistical analysis was performed by one-way ANOVA with Bonferroni post-test analysis for each day (B) or at the end of the trial (C). Asterisks indicate levels of statistical significance differences for comparison to H2O/PBS group (*: p < 0.05; ***: p<0.001).
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4595203&req=5

pone.0139935.g006: UV-killed B. bifidum S17 does not protect C57BL/6J mice against DSS-induced colitis.(A) Effect of UV-killed B. bifidum S17/pMGC on DSS-induced weight loss (A) and increase in colonic weight:length ratio (B). Mice were treated with B. bifidum S17/pMGC and challenged with DSS (DSS/S17). Control mice received PBS as placebo and water with or without DSS (DSS/PBS and H2O/PBS respectively, all groups n = 5). Values are mean ± standard error of the mean. Statistical analysis was performed by one-way ANOVA with Bonferroni post-test analysis for each day (B) or at the end of the trial (C). Asterisks indicate levels of statistical significance differences for comparison to H2O/PBS group (*: p < 0.05; ***: p<0.001).
Mentions: Since stable colonization is not required for its probiotic effect, it was further investigated if administration of killed bacteria yields a similar protective effect. To this end, the DSS trial was repeated, however, mice were treated with UV-killed B. bifidum S17/pMGC. Inactivation of B. bifidum S17/pMGC completely abolished the protective affect on DSS-induced weight loss (Fig 6A). Also, the increase in colon weight:length ratio of DSS-challenged, placebo-treated animals compared to the mice receiving H2O and placebo (6.4 ± 0.9 vs. 3.9 ± 0.6 mg/mm) was not prevented by treatment with UV-killed bacteria (6.5 ± 1.0 mg/mm; Fig 6B).

Bottom Line: Colonization of and persistence in the gastrointestinal tract is thus contributing to the beneficial effects of these strains.Conversely, B. bifidum S17/pMGC, i.e., a strain of human origin, adhered at significantly higher levels to human compared to murine IECs (p < 0.001).Collectively, these results suggest a selective disadvantage of B. bifidum S17/pMGC in the competition with the normal murine microbiota and an anti-inflammatory effect that requires live, metabolically active bacteria.

View Article: PubMed Central - PubMed

Affiliation: Institute of Microbiology and Biotechnology, University of Ulm, 89068, Ulm, Germany.

ABSTRACT
The effects of at least some probiotics are restricted to live, metabolically active bacteria at their site of action. Colonization of and persistence in the gastrointestinal tract is thus contributing to the beneficial effects of these strains. In the present study, colonization of an anti-inflammatory Bifidobacterium bifidum strain was studied in C57BL/6J mice under germ-free (GF) and specific pathogen-free (SPF) conditions as well as during dextran sulfate sodium (DSS)-induced colitis. B. bifidum S17/pMGC was unable to stably colonize C57BL/6J mice under SPF conditions. Mono-association of GF mice by three doses on consecutive days led to long-term, stable detection of up to 109 colony forming units (CFU) of B. bifidum S17/pMGC per g feces. This stable population was rapidly outcompeted upon transfer of mono-associated animals to SPF conditions. A B. animalis strain was isolated from the microbiota of these re-conventionalized mice. This B. animalis strain displayed significantly higher adhesion to murine CMT-93 intestinal epithelial cells (IECs) than to human Caco-2 IECs (p = 0.018). Conversely, B. bifidum S17/pMGC, i.e., a strain of human origin, adhered at significantly higher levels to human compared to murine IECs (p < 0.001). Disturbance of the gut ecology and induction of colitis by DSS-treatment did not promote colonization of the murine gastrointestinal tract (GIT) by B. bifidum S17/pMGC. Despite its poor colonization of the mouse GIT, B. bifidum S17/pMGC displayed a protective effect on DSS-induced colitis when administered as viable bacteria but not as UV-inactivated preparation. Collectively, these results suggest a selective disadvantage of B. bifidum S17/pMGC in the competition with the normal murine microbiota and an anti-inflammatory effect that requires live, metabolically active bacteria.

No MeSH data available.


Related in: MedlinePlus