Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice
Purpose Fructooligosaccharides (FOS) are used as functional foods due to their prebiotic effects. Intestinal anti-inflammatory activity has been established in most, but not all, studies in animal models of colitis, using mainly chemically induced inflammation. Our goal was to test the effect of FOS...
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| Veröffentlicht in: | European journal of nutrition 2016-06, Vol.55 (4), p.1445-1454 |
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| creator | Capitán-Cañadas, Fermín Ocón, Borja Aranda, Carlos José Anzola, Andrea Suárez, María Dolores Zarzuelo, Antonio de Medina, Fermín Sánchez Martínez-Augustin, Olga |
| description | Purpose
Fructooligosaccharides (FOS) are used as functional foods due to their prebiotic effects. Intestinal anti-inflammatory activity has been established in most, but not all, studies in animal models of colitis, using mainly chemically induced inflammation. Our goal was to test the effect of FOS (degree of polymerization 2–8) in the chronic, lymphocyte-driven CD4+ CD62L+ T cell transfer model of colitis.
Methods
Colitis was induced by transfer of CD4+ CD62L+ T cells to C57BL/6J Rag1
−/−
mice. FOS (75 mg day
−1
) was administered by gavage as a post-treatment. Three groups were established: non-colitic (NC), colitic control (C, CD4+ CD62L+ transferred mice treated with vehicle) and colitic+FOS (C+FOS, similar but treated with FOS). Mice were killed after 13 days.
Results
Treatment of mice with FOS ameliorated colitis, as evidenced by an increase in body weight, a lesser myeloperoxidase and alkaline phosphatase activities, a lower secretion of proinflammatory cytokines by mesenteric lymph node cells ex vivo (IFN-γ, IL-17, and TNF-α), and a higher colonic expression of occludin (C+FOS vs. C,
p
|
| doi_str_mv | 10.1007/s00394-015-0962-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1811908326</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4062876161</sourcerecordid><originalsourceid>FETCH-LOGICAL-c405t-15f7dc01645fd5de1c6cd379f281260a7ee2a16fc294c17916eb518e94f11ea43</originalsourceid><addsrcrecordid>eNqFkd9qFTEQxoNYbK0-gDcS8EYo22ay-XP2Uo9WKwe8qdchzU7alN1NTbLieQJf2yxbiwjFmyQwv--bmXyEvAJ2Cozps8xY24mGgWxYp3ijnpAjEK1qFAf59OHN9CF5nvMtY4y3Cp6RQ65ACq3VEfl1nmZXYhzCdczWuRubQo-Z4k9MhYapYC5hsgO1UwlNmPxgx9GWmPbUuhJ-hLKvFC03SLcfxEk9FN-d0EvqcBhoSXbKHhMdY48DjZ662qmEvGi2Ur_fnakvdAwOX5ADb4eML-_vY_Lt_OPl9nOz-_rpYvtu1zjBZGlAet07BkpI38sewSnXt7rzfANcMasRuQXlHe-EA92BwisJG-yEB0Ar2mPydvW9S_H7XJczY8jLrHbCOGcDG4CObVqu_o_qjgmlWsUr-uYf9DbOqX7bSoFsgbNKwUq5FHNO6M1dCqNNewPMLIGaNVBTBWYJ1CxDvL53nq9G7B8UfxKsAF-BXEvTNaa_Wj_q-hsJtalZ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1790153120</pqid></control><display><type>article</type><title>Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Capitán-Cañadas, Fermín ; Ocón, Borja ; Aranda, Carlos José ; Anzola, Andrea ; Suárez, María Dolores ; Zarzuelo, Antonio ; de Medina, Fermín Sánchez ; Martínez-Augustin, Olga</creator><creatorcontrib>Capitán-Cañadas, Fermín ; Ocón, Borja ; Aranda, Carlos José ; Anzola, Andrea ; Suárez, María Dolores ; Zarzuelo, Antonio ; de Medina, Fermín Sánchez ; Martínez-Augustin, Olga</creatorcontrib><description>Purpose
Fructooligosaccharides (FOS) are used as functional foods due to their prebiotic effects. Intestinal anti-inflammatory activity has been established in most, but not all, studies in animal models of colitis, using mainly chemically induced inflammation. Our goal was to test the effect of FOS (degree of polymerization 2–8) in the chronic, lymphocyte-driven CD4+ CD62L+ T cell transfer model of colitis.
Methods
Colitis was induced by transfer of CD4+ CD62L+ T cells to C57BL/6J Rag1
−/−
mice. FOS (75 mg day
−1
) was administered by gavage as a post-treatment. Three groups were established: non-colitic (NC), colitic control (C, CD4+ CD62L+ transferred mice treated with vehicle) and colitic+FOS (C+FOS, similar but treated with FOS). Mice were killed after 13 days.
Results
Treatment of mice with FOS ameliorated colitis, as evidenced by an increase in body weight, a lesser myeloperoxidase and alkaline phosphatase activities, a lower secretion of proinflammatory cytokines by mesenteric lymph node cells ex vivo (IFN-γ, IL-17, and TNF-α), and a higher colonic expression of occludin (C+FOS vs. C,
p
< 0.05). Increased relative abundance of lactic acid bacteria was observed in FOS-treated mice (
p
< 0.05).
Conclusions
FOS exert intestinal anti-inflammatory activity in T lymphocyte-dependent colitis, suggesting it may be useful in the management of inflammatory bowel disease in appropriate conditions.</description><identifier>ISSN: 1436-6207</identifier><identifier>EISSN: 1436-6215</identifier><identifier>DOI: 10.1007/s00394-015-0962-6</identifier><identifier>PMID: 26154776</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Alkaline Phosphatase - metabolism ; Animals ; Anti-Inflammatory Agents - pharmacology ; Calgranulin A - genetics ; Calgranulin A - metabolism ; CD4-Positive T-Lymphocytes - metabolism ; Chemistry ; Chemistry and Materials Science ; Claudin-4 - genetics ; Claudin-4 - metabolism ; Claudin-5 - genetics ; Claudin-5 - metabolism ; Colitis - drug therapy ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Female ; Gastrointestinal Microbiome ; Gene Expression Regulation ; Interferon-gamma - genetics ; Interferon-gamma - metabolism ; Interleukin-10 - genetics ; Interleukin-10 - metabolism ; Interleukin-17 - genetics ; Interleukin-17 - metabolism ; Interleukin-1beta - genetics ; Interleukin-1beta - metabolism ; Intestines - drug effects ; Intestines - metabolism ; Intestines - microbiology ; L-Selectin - metabolism ; Lactobacillus ; Mice ; Mice, Inbred C57BL ; Nutrition ; Occludin - genetics ; Occludin - metabolism ; Oligosaccharides - pharmacology ; Original Contribution ; Peroxidase - metabolism ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>European journal of nutrition, 2016-06, Vol.55 (4), p.1445-1454</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-15f7dc01645fd5de1c6cd379f281260a7ee2a16fc294c17916eb518e94f11ea43</citedby><cites>FETCH-LOGICAL-c405t-15f7dc01645fd5de1c6cd379f281260a7ee2a16fc294c17916eb518e94f11ea43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00394-015-0962-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00394-015-0962-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26154776$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Capitán-Cañadas, Fermín</creatorcontrib><creatorcontrib>Ocón, Borja</creatorcontrib><creatorcontrib>Aranda, Carlos José</creatorcontrib><creatorcontrib>Anzola, Andrea</creatorcontrib><creatorcontrib>Suárez, María Dolores</creatorcontrib><creatorcontrib>Zarzuelo, Antonio</creatorcontrib><creatorcontrib>de Medina, Fermín Sánchez</creatorcontrib><creatorcontrib>Martínez-Augustin, Olga</creatorcontrib><title>Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice</title><title>European journal of nutrition</title><addtitle>Eur J Nutr</addtitle><addtitle>Eur J Nutr</addtitle><description>Purpose
Fructooligosaccharides (FOS) are used as functional foods due to their prebiotic effects. Intestinal anti-inflammatory activity has been established in most, but not all, studies in animal models of colitis, using mainly chemically induced inflammation. Our goal was to test the effect of FOS (degree of polymerization 2–8) in the chronic, lymphocyte-driven CD4+ CD62L+ T cell transfer model of colitis.
Methods
Colitis was induced by transfer of CD4+ CD62L+ T cells to C57BL/6J Rag1
−/−
mice. FOS (75 mg day
−1
) was administered by gavage as a post-treatment. Three groups were established: non-colitic (NC), colitic control (C, CD4+ CD62L+ transferred mice treated with vehicle) and colitic+FOS (C+FOS, similar but treated with FOS). Mice were killed after 13 days.
Results
Treatment of mice with FOS ameliorated colitis, as evidenced by an increase in body weight, a lesser myeloperoxidase and alkaline phosphatase activities, a lower secretion of proinflammatory cytokines by mesenteric lymph node cells ex vivo (IFN-γ, IL-17, and TNF-α), and a higher colonic expression of occludin (C+FOS vs. C,
p
< 0.05). Increased relative abundance of lactic acid bacteria was observed in FOS-treated mice (
p
< 0.05).
Conclusions
FOS exert intestinal anti-inflammatory activity in T lymphocyte-dependent colitis, suggesting it may be useful in the management of inflammatory bowel disease in appropriate conditions.</description><subject>Alkaline Phosphatase - metabolism</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Calgranulin A - genetics</subject><subject>Calgranulin A - metabolism</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Claudin-4 - genetics</subject><subject>Claudin-4 - metabolism</subject><subject>Claudin-5 - genetics</subject><subject>Claudin-5 - metabolism</subject><subject>Colitis - drug therapy</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Gastrointestinal Microbiome</subject><subject>Gene Expression Regulation</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-10 - metabolism</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-17 - metabolism</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>Intestines - drug effects</subject><subject>Intestines - metabolism</subject><subject>Intestines - microbiology</subject><subject>L-Selectin - metabolism</subject><subject>Lactobacillus</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Nutrition</subject><subject>Occludin - genetics</subject><subject>Occludin - metabolism</subject><subject>Oligosaccharides - pharmacology</subject><subject>Original Contribution</subject><subject>Peroxidase - metabolism</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1436-6207</issn><issn>1436-6215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNqFkd9qFTEQxoNYbK0-gDcS8EYo22ay-XP2Uo9WKwe8qdchzU7alN1NTbLieQJf2yxbiwjFmyQwv--bmXyEvAJ2Cozps8xY24mGgWxYp3ijnpAjEK1qFAf59OHN9CF5nvMtY4y3Cp6RQ65ACq3VEfl1nmZXYhzCdczWuRubQo-Z4k9MhYapYC5hsgO1UwlNmPxgx9GWmPbUuhJ-hLKvFC03SLcfxEk9FN-d0EvqcBhoSXbKHhMdY48DjZ662qmEvGi2Ur_fnakvdAwOX5ADb4eML-_vY_Lt_OPl9nOz-_rpYvtu1zjBZGlAet07BkpI38sewSnXt7rzfANcMasRuQXlHe-EA92BwisJG-yEB0Ar2mPydvW9S_H7XJczY8jLrHbCOGcDG4CObVqu_o_qjgmlWsUr-uYf9DbOqX7bSoFsgbNKwUq5FHNO6M1dCqNNewPMLIGaNVBTBWYJ1CxDvL53nq9G7B8UfxKsAF-BXEvTNaa_Wj_q-hsJtalZ</recordid><startdate>20160601</startdate><enddate>20160601</enddate><creator>Capitán-Cañadas, Fermín</creator><creator>Ocón, Borja</creator><creator>Aranda, Carlos José</creator><creator>Anzola, Andrea</creator><creator>Suárez, María Dolores</creator><creator>Zarzuelo, Antonio</creator><creator>de Medina, Fermín Sánchez</creator><creator>Martínez-Augustin, Olga</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>7QP</scope><scope>7RQ</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20160601</creationdate><title>Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice</title><author>Capitán-Cañadas, Fermín ; Ocón, Borja ; Aranda, Carlos José ; Anzola, Andrea ; Suárez, María Dolores ; Zarzuelo, Antonio ; de Medina, Fermín Sánchez ; Martínez-Augustin, Olga</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-15f7dc01645fd5de1c6cd379f281260a7ee2a16fc294c17916eb518e94f11ea43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Calgranulin A - genetics</topic><topic>Calgranulin A - metabolism</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Claudin-4 - genetics</topic><topic>Claudin-4 - metabolism</topic><topic>Claudin-5 - genetics</topic><topic>Claudin-5 - metabolism</topic><topic>Colitis - drug therapy</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>Gastrointestinal Microbiome</topic><topic>Gene Expression Regulation</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-10 - metabolism</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-17 - metabolism</topic><topic>Interleukin-1beta - genetics</topic><topic>Interleukin-1beta - metabolism</topic><topic>Intestines - drug effects</topic><topic>Intestines - metabolism</topic><topic>Intestines - microbiology</topic><topic>L-Selectin - metabolism</topic><topic>Lactobacillus</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Nutrition</topic><topic>Occludin - genetics</topic><topic>Occludin - metabolism</topic><topic>Oligosaccharides - pharmacology</topic><topic>Original Contribution</topic><topic>Peroxidase - metabolism</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Capitán-Cañadas, Fermín</creatorcontrib><creatorcontrib>Ocón, Borja</creatorcontrib><creatorcontrib>Aranda, Carlos José</creatorcontrib><creatorcontrib>Anzola, Andrea</creatorcontrib><creatorcontrib>Suárez, María Dolores</creatorcontrib><creatorcontrib>Zarzuelo, Antonio</creatorcontrib><creatorcontrib>de Medina, Fermín Sánchez</creatorcontrib><creatorcontrib>Martínez-Augustin, Olga</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>Calcium & Calcified Tissue Abstracts</collection><collection>Career & Technical Education Database</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Capitán-Cañadas, Fermín</au><au>Ocón, Borja</au><au>Aranda, Carlos José</au><au>Anzola, Andrea</au><au>Suárez, María Dolores</au><au>Zarzuelo, Antonio</au><au>de Medina, Fermín Sánchez</au><au>Martínez-Augustin, Olga</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice</atitle><jtitle>European journal of nutrition</jtitle><stitle>Eur J Nutr</stitle><addtitle>Eur J Nutr</addtitle><date>2016-06-01</date><risdate>2016</risdate><volume>55</volume><issue>4</issue><spage>1445</spage><epage>1454</epage><pages>1445-1454</pages><issn>1436-6207</issn><eissn>1436-6215</eissn><abstract>Purpose
Fructooligosaccharides (FOS) are used as functional foods due to their prebiotic effects. Intestinal anti-inflammatory activity has been established in most, but not all, studies in animal models of colitis, using mainly chemically induced inflammation. Our goal was to test the effect of FOS (degree of polymerization 2–8) in the chronic, lymphocyte-driven CD4+ CD62L+ T cell transfer model of colitis.
Methods
Colitis was induced by transfer of CD4+ CD62L+ T cells to C57BL/6J Rag1
−/−
mice. FOS (75 mg day
−1
) was administered by gavage as a post-treatment. Three groups were established: non-colitic (NC), colitic control (C, CD4+ CD62L+ transferred mice treated with vehicle) and colitic+FOS (C+FOS, similar but treated with FOS). Mice were killed after 13 days.
Results
Treatment of mice with FOS ameliorated colitis, as evidenced by an increase in body weight, a lesser myeloperoxidase and alkaline phosphatase activities, a lower secretion of proinflammatory cytokines by mesenteric lymph node cells ex vivo (IFN-γ, IL-17, and TNF-α), and a higher colonic expression of occludin (C+FOS vs. C,
p
< 0.05). Increased relative abundance of lactic acid bacteria was observed in FOS-treated mice (
p
< 0.05).
Conclusions
FOS exert intestinal anti-inflammatory activity in T lymphocyte-dependent colitis, suggesting it may be useful in the management of inflammatory bowel disease in appropriate conditions.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26154776</pmid><doi>10.1007/s00394-015-0962-6</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1436-6207 |
| ispartof | European journal of nutrition, 2016-06, Vol.55 (4), p.1445-1454 |
| issn | 1436-6207 1436-6215 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Alkaline Phosphatase - metabolism Animals Anti-Inflammatory Agents - pharmacology Calgranulin A - genetics Calgranulin A - metabolism CD4-Positive T-Lymphocytes - metabolism Chemistry Chemistry and Materials Science Claudin-4 - genetics Claudin-4 - metabolism Claudin-5 - genetics Claudin-5 - metabolism Colitis - drug therapy Disease Models, Animal Dose-Response Relationship, Drug Female Gastrointestinal Microbiome Gene Expression Regulation Interferon-gamma - genetics Interferon-gamma - metabolism Interleukin-10 - genetics Interleukin-10 - metabolism Interleukin-17 - genetics Interleukin-17 - metabolism Interleukin-1beta - genetics Interleukin-1beta - metabolism Intestines - drug effects Intestines - metabolism Intestines - microbiology L-Selectin - metabolism Lactobacillus Mice Mice, Inbred C57BL Nutrition Occludin - genetics Occludin - metabolism Oligosaccharides - pharmacology Original Contribution Peroxidase - metabolism Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism |
| title | Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice |
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