Lactobacillus rhamnosus GG supernatant promotes intestinal barrier function, balances Treg and TH17 cells and ameliorates hepatic injury in a mouse model of chronic-binge alcohol feeding
•LGG supernatant ameliorates experimental ALD in a chronic-binge alcohol exposure model.•LGG supernatant normalizes the balance of Treg and TH17 in peripheral blood of mice exposed to chronic-binge alcohol.•LGG supernatant decreases the serum level of IL-17 in chronic-binge alcohol mice model. Impai...
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Veröffentlicht in: | Toxicology letters 2016-01, Vol.241, p.103-110 |
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creator | Chen, Rui-Cong Xu, Lan-Man Du, Shan-Jie Huang, Si-Si Wu, He Dong, Jia-Jia Huang, Jian-Rong Wang, Xiao-Dong Feng, Wen-Ke Chen, Yong-Ping |
description | •LGG supernatant ameliorates experimental ALD in a chronic-binge alcohol exposure model.•LGG supernatant normalizes the balance of Treg and TH17 in peripheral blood of mice exposed to chronic-binge alcohol.•LGG supernatant decreases the serum level of IL-17 in chronic-binge alcohol mice model.
Impaired intestinal barrier function plays a critical role in alcohol-induced hepatic injury, and the subsequent excessive absorbed endotoxin and bacterial translocation activate the immune response that aggravates the liver injury. Lactobacillus rhamnosus GG supernatant (LGG-s) has been suggested to improve intestinal barrier function and alleviate the liver injury induced by chronic and binge alcohol consumption, but the underlying mechanisms are still not clear. In this study, chronic-binge alcohol fed model was used to determine the effects of LGG-s on the prevention of alcoholic liver disease in C57BL/6 mice and investigate underlying mechanisms. Mice were fed Lieber–DeCarli diet containing 5% alcohol for 10 days, and one dose of alcohol was gavaged on Day 11. In one group, LGG-s was supplemented along with alcohol. Control mice were fed isocaloric diet. Nine hours later the mice were sacrificed for analysis. Chronic-binge alcohol exposure induced an elevation in liver enzymes, steatosis and morphology changes, while LGG-s supplementation attenuated these changes. Treatment with LGG-s significantly improved intestinal barrier function reflected by increased mRNA expression of tight junction (TJ) proteins and villus-crypt histology in ileum, and decreased Escherichia coli (E. coli) protein level in liver. Importantly, flow cytometry analysis showed that alcohol reduced Treg cell population while increased TH17 cell population as well as IL-17 secretion, which was reversed by LGG-s administration. In conclusion, our findings indicate that LGG-s is effective in preventing chronic-binge alcohol exposure-induced liver injury and shed a light on the importance of the balance of Treg and TH17 cells in the role of LGG-s application. |
doi_str_mv | 10.1016/j.toxlet.2015.11.019 |
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Impaired intestinal barrier function plays a critical role in alcohol-induced hepatic injury, and the subsequent excessive absorbed endotoxin and bacterial translocation activate the immune response that aggravates the liver injury. Lactobacillus rhamnosus GG supernatant (LGG-s) has been suggested to improve intestinal barrier function and alleviate the liver injury induced by chronic and binge alcohol consumption, but the underlying mechanisms are still not clear. In this study, chronic-binge alcohol fed model was used to determine the effects of LGG-s on the prevention of alcoholic liver disease in C57BL/6 mice and investigate underlying mechanisms. Mice were fed Lieber–DeCarli diet containing 5% alcohol for 10 days, and one dose of alcohol was gavaged on Day 11. In one group, LGG-s was supplemented along with alcohol. Control mice were fed isocaloric diet. Nine hours later the mice were sacrificed for analysis. Chronic-binge alcohol exposure induced an elevation in liver enzymes, steatosis and morphology changes, while LGG-s supplementation attenuated these changes. Treatment with LGG-s significantly improved intestinal barrier function reflected by increased mRNA expression of tight junction (TJ) proteins and villus-crypt histology in ileum, and decreased Escherichia coli (E. coli) protein level in liver. Importantly, flow cytometry analysis showed that alcohol reduced Treg cell population while increased TH17 cell population as well as IL-17 secretion, which was reversed by LGG-s administration. In conclusion, our findings indicate that LGG-s is effective in preventing chronic-binge alcohol exposure-induced liver injury and shed a light on the importance of the balance of Treg and TH17 cells in the role of LGG-s application.</description><identifier>ISSN: 0378-4274</identifier><identifier>EISSN: 1879-3169</identifier><identifier>DOI: 10.1016/j.toxlet.2015.11.019</identifier><identifier>PMID: 26617183</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alcohol ; Animals ; Binge Drinking - complications ; Binge Drinking - pathology ; Chronic Disease ; Diet ; Escherichia coli Proteins - metabolism ; Fatty Liver, Alcoholic - pathology ; Hepatic injury ; Interleukin-17 - biosynthesis ; Intestinal Absorption - drug effects ; Intestinal permeability ; Intestines - cytology ; Intestines - drug effects ; Lactobacillus rhamnosus - chemistry ; Lactobacillus rhamnosus GG supernatant ; Liver - enzymology ; Liver - pathology ; Liver Diseases, Alcoholic - enzymology ; Liver Diseases, Alcoholic - pathology ; Liver Diseases, Alcoholic - prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; T helper 17 cells ; T regulatory cells ; T-Lymphocytes, Regulatory - drug effects ; Th17 Cells - drug effects ; Tight Junction Proteins - biosynthesis</subject><ispartof>Toxicology letters, 2016-01, Vol.241, p.103-110</ispartof><rights>2015 Elsevier Ireland Ltd</rights><rights>Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0001-5456-5347</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.toxlet.2015.11.019$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26617183$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Rui-Cong</creatorcontrib><creatorcontrib>Xu, Lan-Man</creatorcontrib><creatorcontrib>Du, Shan-Jie</creatorcontrib><creatorcontrib>Huang, Si-Si</creatorcontrib><creatorcontrib>Wu, He</creatorcontrib><creatorcontrib>Dong, Jia-Jia</creatorcontrib><creatorcontrib>Huang, Jian-Rong</creatorcontrib><creatorcontrib>Wang, Xiao-Dong</creatorcontrib><creatorcontrib>Feng, Wen-Ke</creatorcontrib><creatorcontrib>Chen, Yong-Ping</creatorcontrib><title>Lactobacillus rhamnosus GG supernatant promotes intestinal barrier function, balances Treg and TH17 cells and ameliorates hepatic injury in a mouse model of chronic-binge alcohol feeding</title><title>Toxicology letters</title><addtitle>Toxicol Lett</addtitle><description>•LGG supernatant ameliorates experimental ALD in a chronic-binge alcohol exposure model.•LGG supernatant normalizes the balance of Treg and TH17 in peripheral blood of mice exposed to chronic-binge alcohol.•LGG supernatant decreases the serum level of IL-17 in chronic-binge alcohol mice model.
Impaired intestinal barrier function plays a critical role in alcohol-induced hepatic injury, and the subsequent excessive absorbed endotoxin and bacterial translocation activate the immune response that aggravates the liver injury. Lactobacillus rhamnosus GG supernatant (LGG-s) has been suggested to improve intestinal barrier function and alleviate the liver injury induced by chronic and binge alcohol consumption, but the underlying mechanisms are still not clear. In this study, chronic-binge alcohol fed model was used to determine the effects of LGG-s on the prevention of alcoholic liver disease in C57BL/6 mice and investigate underlying mechanisms. Mice were fed Lieber–DeCarli diet containing 5% alcohol for 10 days, and one dose of alcohol was gavaged on Day 11. In one group, LGG-s was supplemented along with alcohol. Control mice were fed isocaloric diet. Nine hours later the mice were sacrificed for analysis. Chronic-binge alcohol exposure induced an elevation in liver enzymes, steatosis and morphology changes, while LGG-s supplementation attenuated these changes. Treatment with LGG-s significantly improved intestinal barrier function reflected by increased mRNA expression of tight junction (TJ) proteins and villus-crypt histology in ileum, and decreased Escherichia coli (E. coli) protein level in liver. Importantly, flow cytometry analysis showed that alcohol reduced Treg cell population while increased TH17 cell population as well as IL-17 secretion, which was reversed by LGG-s administration. In conclusion, our findings indicate that LGG-s is effective in preventing chronic-binge alcohol exposure-induced liver injury and shed a light on the importance of the balance of Treg and TH17 cells in the role of LGG-s application.</description><subject>Alcohol</subject><subject>Animals</subject><subject>Binge Drinking - complications</subject><subject>Binge Drinking - pathology</subject><subject>Chronic Disease</subject><subject>Diet</subject><subject>Escherichia coli Proteins - metabolism</subject><subject>Fatty Liver, Alcoholic - pathology</subject><subject>Hepatic injury</subject><subject>Interleukin-17 - biosynthesis</subject><subject>Intestinal Absorption - drug effects</subject><subject>Intestinal permeability</subject><subject>Intestines - cytology</subject><subject>Intestines - drug effects</subject><subject>Lactobacillus rhamnosus - chemistry</subject><subject>Lactobacillus rhamnosus GG supernatant</subject><subject>Liver - enzymology</subject><subject>Liver - pathology</subject><subject>Liver Diseases, Alcoholic - enzymology</subject><subject>Liver Diseases, Alcoholic - pathology</subject><subject>Liver Diseases, Alcoholic - prevention & control</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>T helper 17 cells</subject><subject>T regulatory cells</subject><subject>T-Lymphocytes, Regulatory - drug effects</subject><subject>Th17 Cells - drug effects</subject><subject>Tight Junction Proteins - biosynthesis</subject><issn>0378-4274</issn><issn>1879-3169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1UduKFDEQDaK4s6t_IJIPsNtU3_tFkGWdXRjwZXwO1Un1ToZ00iRpcX_NrzPj6EuduhwOxTmMfQBRgoDu87lM_pelVFYC2hKgFDC-YjsY-rGooRtfs52o-6Foqr65YbcxnoUQXdO1b9lN1XXQw1Dv2O8DquQnVMbaLfJwwsX5mLv9nsdtpeAwoUt8DX7xiSI3LtdkHFo-YQiGAp83p5Lx7lPeWHQqs46Bnjk6zY-P0HNF1sa_Iy5kjQ94UTrRismorHjewksGjnzxW6RcNVnuZ65OwTujism4Z-JolT95y2cinRfv2JsZbaT3__CO_fj2cLx_LA7f90_3Xw8FwQCpGDqtR-prnMZJ1a2eR4GNruoKmx6qqZnauVP9rMZ2qPNpgJ6mSjSDprZtcB7qO_bxqrtu00JarsEsGF7kfxMz4cuVQPmLn9kRGZWh7IM2gVSS2hsJQl5Sk2d5TU1eUpMAMqdW_wFmJZA6</recordid><startdate>20160122</startdate><enddate>20160122</enddate><creator>Chen, Rui-Cong</creator><creator>Xu, Lan-Man</creator><creator>Du, Shan-Jie</creator><creator>Huang, Si-Si</creator><creator>Wu, He</creator><creator>Dong, Jia-Jia</creator><creator>Huang, Jian-Rong</creator><creator>Wang, Xiao-Dong</creator><creator>Feng, Wen-Ke</creator><creator>Chen, Yong-Ping</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><orcidid>https://orcid.org/0000-0001-5456-5347</orcidid></search><sort><creationdate>20160122</creationdate><title>Lactobacillus rhamnosus GG supernatant promotes intestinal barrier function, balances Treg and TH17 cells and ameliorates hepatic injury in a mouse model of chronic-binge alcohol feeding</title><author>Chen, Rui-Cong ; Xu, Lan-Man ; Du, Shan-Jie ; Huang, Si-Si ; Wu, He ; Dong, Jia-Jia ; Huang, Jian-Rong ; Wang, Xiao-Dong ; Feng, Wen-Ke ; Chen, Yong-Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e181t-86dd9e73ab9bc35df90a4d232a4712b4b5f6c7fc958390a817eb2048de554af83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alcohol</topic><topic>Animals</topic><topic>Binge Drinking - complications</topic><topic>Binge Drinking - pathology</topic><topic>Chronic Disease</topic><topic>Diet</topic><topic>Escherichia coli Proteins - metabolism</topic><topic>Fatty Liver, Alcoholic - pathology</topic><topic>Hepatic injury</topic><topic>Interleukin-17 - biosynthesis</topic><topic>Intestinal Absorption - drug effects</topic><topic>Intestinal permeability</topic><topic>Intestines - cytology</topic><topic>Intestines - drug effects</topic><topic>Lactobacillus rhamnosus - chemistry</topic><topic>Lactobacillus rhamnosus GG supernatant</topic><topic>Liver - enzymology</topic><topic>Liver - pathology</topic><topic>Liver Diseases, Alcoholic - enzymology</topic><topic>Liver Diseases, Alcoholic - pathology</topic><topic>Liver Diseases, Alcoholic - prevention & control</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>T helper 17 cells</topic><topic>T regulatory cells</topic><topic>T-Lymphocytes, Regulatory - drug effects</topic><topic>Th17 Cells - drug effects</topic><topic>Tight Junction Proteins - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Rui-Cong</creatorcontrib><creatorcontrib>Xu, Lan-Man</creatorcontrib><creatorcontrib>Du, Shan-Jie</creatorcontrib><creatorcontrib>Huang, Si-Si</creatorcontrib><creatorcontrib>Wu, He</creatorcontrib><creatorcontrib>Dong, Jia-Jia</creatorcontrib><creatorcontrib>Huang, Jian-Rong</creatorcontrib><creatorcontrib>Wang, Xiao-Dong</creatorcontrib><creatorcontrib>Feng, Wen-Ke</creatorcontrib><creatorcontrib>Chen, Yong-Ping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Toxicology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Rui-Cong</au><au>Xu, Lan-Man</au><au>Du, Shan-Jie</au><au>Huang, Si-Si</au><au>Wu, He</au><au>Dong, Jia-Jia</au><au>Huang, Jian-Rong</au><au>Wang, Xiao-Dong</au><au>Feng, Wen-Ke</au><au>Chen, Yong-Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lactobacillus rhamnosus GG supernatant promotes intestinal barrier function, balances Treg and TH17 cells and ameliorates hepatic injury in a mouse model of chronic-binge alcohol feeding</atitle><jtitle>Toxicology letters</jtitle><addtitle>Toxicol Lett</addtitle><date>2016-01-22</date><risdate>2016</risdate><volume>241</volume><spage>103</spage><epage>110</epage><pages>103-110</pages><issn>0378-4274</issn><eissn>1879-3169</eissn><abstract>•LGG supernatant ameliorates experimental ALD in a chronic-binge alcohol exposure model.•LGG supernatant normalizes the balance of Treg and TH17 in peripheral blood of mice exposed to chronic-binge alcohol.•LGG supernatant decreases the serum level of IL-17 in chronic-binge alcohol mice model.
Impaired intestinal barrier function plays a critical role in alcohol-induced hepatic injury, and the subsequent excessive absorbed endotoxin and bacterial translocation activate the immune response that aggravates the liver injury. Lactobacillus rhamnosus GG supernatant (LGG-s) has been suggested to improve intestinal barrier function and alleviate the liver injury induced by chronic and binge alcohol consumption, but the underlying mechanisms are still not clear. In this study, chronic-binge alcohol fed model was used to determine the effects of LGG-s on the prevention of alcoholic liver disease in C57BL/6 mice and investigate underlying mechanisms. Mice were fed Lieber–DeCarli diet containing 5% alcohol for 10 days, and one dose of alcohol was gavaged on Day 11. In one group, LGG-s was supplemented along with alcohol. Control mice were fed isocaloric diet. Nine hours later the mice were sacrificed for analysis. Chronic-binge alcohol exposure induced an elevation in liver enzymes, steatosis and morphology changes, while LGG-s supplementation attenuated these changes. Treatment with LGG-s significantly improved intestinal barrier function reflected by increased mRNA expression of tight junction (TJ) proteins and villus-crypt histology in ileum, and decreased Escherichia coli (E. coli) protein level in liver. Importantly, flow cytometry analysis showed that alcohol reduced Treg cell population while increased TH17 cell population as well as IL-17 secretion, which was reversed by LGG-s administration. In conclusion, our findings indicate that LGG-s is effective in preventing chronic-binge alcohol exposure-induced liver injury and shed a light on the importance of the balance of Treg and TH17 cells in the role of LGG-s application.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26617183</pmid><doi>10.1016/j.toxlet.2015.11.019</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-5456-5347</orcidid></addata></record> |
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subjects | Alcohol Animals Binge Drinking - complications Binge Drinking - pathology Chronic Disease Diet Escherichia coli Proteins - metabolism Fatty Liver, Alcoholic - pathology Hepatic injury Interleukin-17 - biosynthesis Intestinal Absorption - drug effects Intestinal permeability Intestines - cytology Intestines - drug effects Lactobacillus rhamnosus - chemistry Lactobacillus rhamnosus GG supernatant Liver - enzymology Liver - pathology Liver Diseases, Alcoholic - enzymology Liver Diseases, Alcoholic - pathology Liver Diseases, Alcoholic - prevention & control Male Mice Mice, Inbred C57BL T helper 17 cells T regulatory cells T-Lymphocytes, Regulatory - drug effects Th17 Cells - drug effects Tight Junction Proteins - biosynthesis |
title | Lactobacillus rhamnosus GG supernatant promotes intestinal barrier function, balances Treg and TH17 cells and ameliorates hepatic injury in a mouse model of chronic-binge alcohol feeding |
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