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Title of Journal: Eur J Nutr

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Abbravation: European Journal of Nutrition

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Springer Berlin Heidelberg

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DOI

10.1016/0009-2614(85)80929-5

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ISSN

1436-6215

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Emphasis Type="Italic"Lactobacillus/Emphasis G

Authors: Kazutoyo Yoda Kenji Miyazawa Masataka Hosoda Masaru Hiramatsu Fang Yan Fang He
Publish Date: 2013/03/07
Volume: 53, Issue: 1, Pages: 105-115
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Abstract

Fermented milk is considered one of the best sources for efficient consumption of probiotic strains by hosts to promote good health The purpose of this study was to investigate the effects of orally administering LGGfermented milk LGG milk on intestinal inflammation and injury and to study the mechanisms of LGG milk’s actionLGG milk and nonLGGfermented milk nonLGG milk were administered through gavage to mice before and during dextran sodium sulfate DSSinduced intestinal injury and colitis Inflammatory/injury score and colon length were assessed Intestinal epithelial cells were treated with the soluble fraction of LGG milk to detect its effects on the epidermal growth factor receptor EGFR and its downstream target Akt activation cytokineinduced apoptosis and hydrogen peroxide H2O2induced disruption of tight junctionsLGG milk treatment significantly reduced DSSinduced colonic inflammation and injury and colon shortening in mice compared to that in nonLGG milktreated and untreated mice The soluble fraction of LGG milk but not nonLGG milk stimulated the activation of EGFR and Akt in a concentrationdependent manner suppressed cytokineinduced apoptosis and attenuated H2O2induced disruption of tight junction complex in the intestinal epithelial cells These effects of LGG milk were blocked by the EGFR kinase inhibitor LGG milk but not nonLGG milk contained two soluble proteins p40 and p75 that have been reported to promote survival and growth of intestinal epithelial cells through the activation of EGFR Depletion of p40 and p75 from LGG milk abolished the effects of LGG milk on prevention of cytokineinduced apoptosis and H2O2induced disruption of tight junctionsWe thank Ms Ayako Kusanagi Product Development Department at Takanashi Milk Products for kindly providing nonLGG milk and Dr M Kay Washington Department of Pathology Microbiology and Immunology at Vanderbilt University Medical Center for the analysis of colon inflammation and injury This work was supported by Takanashi Milk Products Co Ltd and NIH grants R01DK081134 FY and P30DK058404 Vanderbilt University Digestive Disease Research Center


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