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Enterococcus faecium NCIMB 10415 does not protect interleukin-10 knock-out mice from chronic gut inflammation

In: Beneficial Microbes
Authors:
B.P Ganesh 1German Institute of Human Nutrition Potsdam-Rehbruecke, Department of Gastrointestinal Microbiology, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany

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J.F Richter 2Institute of Clinical Physiology, Charite, Campus Benjamin Franklin, Hindenburgdamm 30, 12203 Berlin, Germany

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M. Blaut 1German Institute of Human Nutrition Potsdam-Rehbruecke, Department of Gastrointestinal Microbiology, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany

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G. Loh 1German Institute of Human Nutrition Potsdam-Rehbruecke, Department of Gastrointestinal Microbiology, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany
loh@dife.de

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Abstract

Enterococcus faecium NCIMB 10415 reduces diarrhoea incidence and duration in animals and human study subjects. We tested whether the strain is also capable of reducing chronic gut inflammation and aimed to identify mechanisms that are involved in possible probiotic effects. To identify health-promoting mechanisms of the strain, we used interleukin-10-deficient mice that spontaneously develop gut inflammation and fed these mice a diet containing NCIMB 10415 for 3, 8 and 24 weeks, respectively. Control mice were fed a diet which was identically composed but did not contain the strain. After 3 weeks of intervention the experimental animals were less inflamed in the caecum than the control animals. This effect was not observed in the colon and there were no differences between experimental and control mice at any other time point. The application of the strain was associated with higher expression levels of interferon gamma and interferon gamma-induced protein 10 after 3 and 24 but not after 8 weeks of feeding. No differences between the animals were observed in intestinal barrier function or intestinal microbiota composition. However, we observed a low abundance of the mucin-degrading bacterium Akkermansia muciniphilain the mice that were fed NCIMB 10415 for 8 weeks. These low cell numbers were associated with a significantly lower caecal inflammation score and improved paracellular permeability as compared to the NCIMB-treated mice that were killed after 3 and 24 weeks of intervention. In conclusion, NCIMB 10415 is not capable of reducing gut inflammation in the IL-10-/- mouse model. The exact role of A. muciniphila and of a possible interaction between this bacterium, NCIMB 10415 and the host in gut inflammation requires further investigation.

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