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Partial Enteral Nutrition Preserves Elements of Gut Barrier Function, Including Innate Immunity, Intestinal Alkaline Phosphatase (IAP) Level, and Intestinal Microbiota in Mice
Lack of enteral nutrition (EN) during parenteral nutrition (PN) leads to higher incidence of infection because of gut barrier dysfunction. However, the effects of partial EN on intestina linnate immunity, intestinal alkaline phosphatase (IAP) and microbiota remain unclear. The mice were randomized i...
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Published in: | Nutrients 2015-08, Vol.7 (8), p.6294-6312 |
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description | Lack of enteral nutrition (EN) during parenteral nutrition (PN) leads to higher incidence of infection because of gut barrier dysfunction. However, the effects of partial EN on intestina linnate immunity, intestinal alkaline phosphatase (IAP) and microbiota remain unclear. The mice were randomized into six groups to receive either standard chow or isocaloric and isonitrogenous nutritional support with variable partial EN to PN ratios. Five days later, the mice were sacrificed and tissue samples were collected. Bacterial translocation, the levels of lysozyme, mucin 2 (MUC2), and IAP were analyzed. The composition of intestinal microbiota was analyzed by 16S rRNA pyrosequencing. Compared with chow, total parenteral nutrition (TPN) resulted in a dysfunctional mucosal barrier, as evidenced by increased bacterial translocation (p < 0.05), loss of lysozyme, MUC2, and IAP, and changes in the gut microbiota (p < 0.001). Administration of 20% EN supplemented with PN significantly increased the concentrations of lysozyme, MUC2, IAP, and the mRNA levels of lysozyme and MUC2 (p < 0.001). The percentages of Bacteroidetes and Tenericutes were significantly lower in the 20% EN group than in the TPN group (p < 0.001). These changes were accompanied by maintained barrier function in bacterial culture (p < 0.05). Supplementation of PN with 20% EN preserves gut barrier function, by way of maintaining innate immunity, IAP and intestinal microbiota. |
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However, the effects of partial EN on intestina linnate immunity, intestinal alkaline phosphatase (IAP) and microbiota remain unclear. The mice were randomized into six groups to receive either standard chow or isocaloric and isonitrogenous nutritional support with variable partial EN to PN ratios. Five days later, the mice were sacrificed and tissue samples were collected. Bacterial translocation, the levels of lysozyme, mucin 2 (MUC2), and IAP were analyzed. The composition of intestinal microbiota was analyzed by 16S rRNA pyrosequencing. Compared with chow, total parenteral nutrition (TPN) resulted in a dysfunctional mucosal barrier, as evidenced by increased bacterial translocation (p < 0.05), loss of lysozyme, MUC2, and IAP, and changes in the gut microbiota (p < 0.001). Administration of 20% EN supplemented with PN significantly increased the concentrations of lysozyme, MUC2, IAP, and the mRNA levels of lysozyme and MUC2 (p < 0.001). The percentages of Bacteroidetes and Tenericutes were significantly lower in the 20% EN group than in the TPN group (p < 0.001). These changes were accompanied by maintained barrier function in bacterial culture (p < 0.05). Supplementation of PN with 20% EN preserves gut barrier function, by way of maintaining innate immunity, IAP and intestinal microbiota.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu7085288</identifier><identifier>PMID: 26247961</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Alkaline Phosphatase - metabolism ; Animals ; Bacteria ; Bacterial Translocation ; Bacteroidetes ; Clinical outcomes ; Enteral Nutrition ; Gastrointestinal Microbiome - genetics ; gut barrier ; Immunity, Innate ; innate immunity ; intestinal alkaline phosphatase ; intestinal microbiota ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - microbiology ; Intestinal Mucosa - pathology ; Intestines - metabolism ; Intestines - microbiology ; Intestines - pathology ; Laboratory animals ; Male ; Medical research ; Mice ; Microbiota ; Mucin-2 - genetics ; Mucin-2 - metabolism ; Muramidase - genetics ; Muramidase - metabolism ; Nutrition ; Parenteral nutrition ; Parenteral Nutrition - methods ; Parenteral Nutrition, Total ; partial enteral nutrition ; Phosphatase ; RNA, Messenger - metabolism ; RNA, Ribosomal, 16S ; Tenericutes</subject><ispartof>Nutrients, 2015-08, Vol.7 (8), p.6294-6312</ispartof><rights>Copyright MDPI AG 2015</rights><rights>2015 by the authors; licensee MDPI, Basel, Switzerland. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c568t-c03940f5318c9d43e316634ed194a924420d6a506a54a38113b0ab7fbeae25003</citedby><cites>FETCH-LOGICAL-c568t-c03940f5318c9d43e316634ed194a924420d6a506a54a38113b0ab7fbeae25003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1729218025/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1729218025?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26247961$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wan, Xiao</creatorcontrib><creatorcontrib>Bi, Jingcheng</creatorcontrib><creatorcontrib>Gao, Xuejin</creatorcontrib><creatorcontrib>Tian, Feng</creatorcontrib><creatorcontrib>Wang, Xinying</creatorcontrib><creatorcontrib>Li, Ning</creatorcontrib><creatorcontrib>Li, Jieshou</creatorcontrib><title>Partial Enteral Nutrition Preserves Elements of Gut Barrier Function, Including Innate Immunity, Intestinal Alkaline Phosphatase (IAP) Level, and Intestinal Microbiota in Mice</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>Lack of enteral nutrition (EN) during parenteral nutrition (PN) leads to higher incidence of infection because of gut barrier dysfunction. However, the effects of partial EN on intestina linnate immunity, intestinal alkaline phosphatase (IAP) and microbiota remain unclear. The mice were randomized into six groups to receive either standard chow or isocaloric and isonitrogenous nutritional support with variable partial EN to PN ratios. Five days later, the mice were sacrificed and tissue samples were collected. Bacterial translocation, the levels of lysozyme, mucin 2 (MUC2), and IAP were analyzed. The composition of intestinal microbiota was analyzed by 16S rRNA pyrosequencing. Compared with chow, total parenteral nutrition (TPN) resulted in a dysfunctional mucosal barrier, as evidenced by increased bacterial translocation (p < 0.05), loss of lysozyme, MUC2, and IAP, and changes in the gut microbiota (p < 0.001). Administration of 20% EN supplemented with PN significantly increased the concentrations of lysozyme, MUC2, IAP, and the mRNA levels of lysozyme and MUC2 (p < 0.001). The percentages of Bacteroidetes and Tenericutes were significantly lower in the 20% EN group than in the TPN group (p < 0.001). These changes were accompanied by maintained barrier function in bacterial culture (p < 0.05). Supplementation of PN with 20% EN preserves gut barrier function, by way of maintaining innate immunity, IAP and intestinal microbiota.</description><subject>Alkaline Phosphatase - metabolism</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Bacterial Translocation</subject><subject>Bacteroidetes</subject><subject>Clinical outcomes</subject><subject>Enteral Nutrition</subject><subject>Gastrointestinal Microbiome - genetics</subject><subject>gut barrier</subject><subject>Immunity, Innate</subject><subject>innate immunity</subject><subject>intestinal alkaline phosphatase</subject><subject>intestinal microbiota</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - microbiology</subject><subject>Intestinal Mucosa - pathology</subject><subject>Intestines - metabolism</subject><subject>Intestines - microbiology</subject><subject>Intestines - pathology</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Medical research</subject><subject>Mice</subject><subject>Microbiota</subject><subject>Mucin-2 - genetics</subject><subject>Mucin-2 - metabolism</subject><subject>Muramidase - genetics</subject><subject>Muramidase - metabolism</subject><subject>Nutrition</subject><subject>Parenteral nutrition</subject><subject>Parenteral Nutrition - methods</subject><subject>Parenteral Nutrition, Total</subject><subject>partial enteral nutrition</subject><subject>Phosphatase</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Ribosomal, 16S</subject><subject>Tenericutes</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqNkt9u0zAUxiMEYtPYBS-ALHGzSSs4_hvfIJWpG5EK9AKuIyc5aV0Su9hOpT0Vr4hDR9VxhSXLxz4_f_L5fLLsdY7fUarweztKXHBSFM-yc4IlmQnB6POT-Cy7DGGLpyGxFPRldkYEYVKJ_Dz7tdI-Gt2jhY3g0_pljN5E4yxaeQjg9xDQoocBbAzIdeh-jOij9t6AR3ejbSb0BpW26cfW2HWKrI6AymEYrYkPUypCiMYm7Xn_Q_fGAlptXNhtdNQB0FU5X12jJeyhv0HatqcXPpvGu9q4qJGx0w5eZS863Qe4fFwvsu93i2-3n2bLr_fl7Xw5a7go4qzBVDHccZoXjWoZBZoLQRm0uWJaEcYIboXmOE2maZHntMa6ll0NGgjHmF5k5UG3dXpb7bwZtH-onDbVnwPn19VkXNNDJamiFASnlBdMaV4TToSsO90RpmsFSevDQWs31gO0TbIyOf1E9GnGmk21dvuKcc5zIpPA1aOAdz_HZE41mNBA32sLbgxVXpBUrmTyP1CJieBKqAl9-w-6daNPtk8UUSQvMOGJuj5Q6SdC8NAd353jamrA6tiAiX1zWuiR_Ntu9DcBgdXv</recordid><startdate>20150803</startdate><enddate>20150803</enddate><creator>Wan, Xiao</creator><creator>Bi, Jingcheng</creator><creator>Gao, Xuejin</creator><creator>Tian, Feng</creator><creator>Wang, Xinying</creator><creator>Li, Ning</creator><creator>Li, Jieshou</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150803</creationdate><title>Partial Enteral Nutrition Preserves Elements of Gut Barrier Function, Including Innate Immunity, Intestinal Alkaline Phosphatase (IAP) Level, and Intestinal Microbiota in Mice</title><author>Wan, Xiao ; Bi, Jingcheng ; Gao, Xuejin ; Tian, Feng ; Wang, Xinying ; Li, Ning ; Li, Jieshou</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c568t-c03940f5318c9d43e316634ed194a924420d6a506a54a38113b0ab7fbeae25003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Bacterial Translocation</topic><topic>Bacteroidetes</topic><topic>Clinical outcomes</topic><topic>Enteral Nutrition</topic><topic>Gastrointestinal Microbiome - genetics</topic><topic>gut barrier</topic><topic>Immunity, Innate</topic><topic>innate immunity</topic><topic>intestinal alkaline phosphatase</topic><topic>intestinal microbiota</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - microbiology</topic><topic>Intestinal Mucosa - pathology</topic><topic>Intestines - metabolism</topic><topic>Intestines - microbiology</topic><topic>Intestines - pathology</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Medical research</topic><topic>Mice</topic><topic>Microbiota</topic><topic>Mucin-2 - genetics</topic><topic>Mucin-2 - metabolism</topic><topic>Muramidase - genetics</topic><topic>Muramidase - metabolism</topic><topic>Nutrition</topic><topic>Parenteral nutrition</topic><topic>Parenteral Nutrition - methods</topic><topic>Parenteral Nutrition, Total</topic><topic>partial enteral nutrition</topic><topic>Phosphatase</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Ribosomal, 16S</topic><topic>Tenericutes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wan, Xiao</creatorcontrib><creatorcontrib>Bi, Jingcheng</creatorcontrib><creatorcontrib>Gao, Xuejin</creatorcontrib><creatorcontrib>Tian, Feng</creatorcontrib><creatorcontrib>Wang, Xinying</creatorcontrib><creatorcontrib>Li, Ning</creatorcontrib><creatorcontrib>Li, Jieshou</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wan, Xiao</au><au>Bi, Jingcheng</au><au>Gao, Xuejin</au><au>Tian, Feng</au><au>Wang, Xinying</au><au>Li, Ning</au><au>Li, Jieshou</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Partial Enteral Nutrition Preserves Elements of Gut Barrier Function, Including Innate Immunity, Intestinal Alkaline Phosphatase (IAP) Level, and Intestinal Microbiota in Mice</atitle><jtitle>Nutrients</jtitle><addtitle>Nutrients</addtitle><date>2015-08-03</date><risdate>2015</risdate><volume>7</volume><issue>8</issue><spage>6294</spage><epage>6312</epage><pages>6294-6312</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>Lack of enteral nutrition (EN) during parenteral nutrition (PN) leads to higher incidence of infection because of gut barrier dysfunction. However, the effects of partial EN on intestina linnate immunity, intestinal alkaline phosphatase (IAP) and microbiota remain unclear. The mice were randomized into six groups to receive either standard chow or isocaloric and isonitrogenous nutritional support with variable partial EN to PN ratios. Five days later, the mice were sacrificed and tissue samples were collected. Bacterial translocation, the levels of lysozyme, mucin 2 (MUC2), and IAP were analyzed. The composition of intestinal microbiota was analyzed by 16S rRNA pyrosequencing. Compared with chow, total parenteral nutrition (TPN) resulted in a dysfunctional mucosal barrier, as evidenced by increased bacterial translocation (p < 0.05), loss of lysozyme, MUC2, and IAP, and changes in the gut microbiota (p < 0.001). Administration of 20% EN supplemented with PN significantly increased the concentrations of lysozyme, MUC2, IAP, and the mRNA levels of lysozyme and MUC2 (p < 0.001). The percentages of Bacteroidetes and Tenericutes were significantly lower in the 20% EN group than in the TPN group (p < 0.001). These changes were accompanied by maintained barrier function in bacterial culture (p < 0.05). Supplementation of PN with 20% EN preserves gut barrier function, by way of maintaining innate immunity, IAP and intestinal microbiota.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>26247961</pmid><doi>10.3390/nu7085288</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alkaline Phosphatase - metabolism Animals Bacteria Bacterial Translocation Bacteroidetes Clinical outcomes Enteral Nutrition Gastrointestinal Microbiome - genetics gut barrier Immunity, Innate innate immunity intestinal alkaline phosphatase intestinal microbiota Intestinal Mucosa - metabolism Intestinal Mucosa - microbiology Intestinal Mucosa - pathology Intestines - metabolism Intestines - microbiology Intestines - pathology Laboratory animals Male Medical research Mice Microbiota Mucin-2 - genetics Mucin-2 - metabolism Muramidase - genetics Muramidase - metabolism Nutrition Parenteral nutrition Parenteral Nutrition - methods Parenteral Nutrition, Total partial enteral nutrition Phosphatase RNA, Messenger - metabolism RNA, Ribosomal, 16S Tenericutes |
title | Partial Enteral Nutrition Preserves Elements of Gut Barrier Function, Including Innate Immunity, Intestinal Alkaline Phosphatase (IAP) Level, and Intestinal Microbiota in Mice |
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