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Alanyl-glutamine administration suppresses Th17 and reduces inflammatory reaction in dextran sulfate sodium-induced acute colitis
T helper (Th) cells play a major role in the pathogenesis of inflammatory bowel disease (IBD). Glutamine (Gln) is known to have immunomodulatory effects in metabolic stressed conditions. This study investigated the effects of post-treatment of alanyl-glutamine (Ala-Gln) on Th cell-associated cytokin...
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| Published in: | International immunopharmacology 2013-09, Vol.17 (1), p.1-8 |
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| description | T helper (Th) cells play a major role in the pathogenesis of inflammatory bowel disease (IBD). Glutamine (Gln) is known to have immunomodulatory effects in metabolic stressed conditions. This study investigated the effects of post-treatment of alanyl-glutamine (Ala-Gln) on Th cell-associated cytokine expressions and inflammatory reaction in dextran sulfate sodium (DSS)-induced colitis. C57BL/6 mice received distilled water containing 3% DSS for 5days to induce colitis, whereas the normal control (NC) group received distilled water. After induction of colitis, one of the colitis groups (DG) was intraperitoneally injected with an Ala-Gln solution (0.5gGln/kg/d), and the saline DSS group (DS) received an identical volume of saline. After treatment for 3days, mice were sacrificed, and the blood and tissue samples were collected for further analysis. DSS colitis resulted in higher percentages of blood interleukin (IL)-17-secreting Th cells and greater expression of Th cell-associated cytokine messenger RNA (mRNA) in the mesenteric lymph nodes (MLN). Also, luminal immunoglobin (Ig) G, keratinocyte-derived chemokine, and macrophage chemoattractant protein-1 levels were higher in the DS group than the NC group, whereas these parameters did not differ between the DG and NC groups. The DG group had lower blood IL-17A, 17F, MLN IL-17 mRNA and macrophage percentage in the peritoneal lavage fluid than those of the DS group. These results suggest that post-treatment with Ala-Gln suppressed Th17-associated cytokine expressions, reduced macrophage infiltration into the peritoneal cavity and decreased pro-inflammatory cytokine production in the colon, thus may have attenuated inflammatory response in DSS-induced colitis.
•Post-treatment with Ala-Gln attenuated inflammatory response in a model of colitis.•Ala-Gln administration suppressed Th17-associated cytokine production.•Ala-Gln reduced macrophage infiltration and pro-inflammatory cytokine production. |
| doi_str_mv | 10.1016/j.intimp.2013.05.004 |
| format | article |
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•Post-treatment with Ala-Gln attenuated inflammatory response in a model of colitis.•Ala-Gln administration suppressed Th17-associated cytokine production.•Ala-Gln reduced macrophage infiltration and pro-inflammatory cytokine production.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2013.05.004</identifier><identifier>PMID: 23721689</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Alanyl-glutamine ; Animals ; Body Weight ; Colitis - chemically induced ; Colitis - drug therapy ; Colon ; Cytokines - genetics ; Cytokines - metabolism ; Dextran Sulfate - toxicity ; Dipeptides - therapeutic use ; DSS-colitis ; Gene Expression Regulation - drug effects ; Immunoglobin G ; Inflammation - chemically induced ; Inflammation - drug therapy ; Interleukin-17 ; Male ; Mice ; Mice, Inbred C57BL ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; T helper cells ; Th17 Cells - drug effects ; Th17 Cells - physiology</subject><ispartof>International immunopharmacology, 2013-09, Vol.17 (1), p.1-8</ispartof><rights>2013 Elsevier B.V.</rights><rights>Copyright © 2013 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-5025c67e93f227cbf7b9a3e480dbcfcba6fa4567dc72b886aabd60a238d6996d3</citedby><cites>FETCH-LOGICAL-c461t-5025c67e93f227cbf7b9a3e480dbcfcba6fa4567dc72b886aabd60a238d6996d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23721689$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hou, Yu-Chen</creatorcontrib><creatorcontrib>Liu, Jun-Jen</creatorcontrib><creatorcontrib>Pai, Man-Hui</creatorcontrib><creatorcontrib>Tsou, Shung-Sheng</creatorcontrib><creatorcontrib>Yeh, Sung-Ling</creatorcontrib><title>Alanyl-glutamine administration suppresses Th17 and reduces inflammatory reaction in dextran sulfate sodium-induced acute colitis</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>T helper (Th) cells play a major role in the pathogenesis of inflammatory bowel disease (IBD). Glutamine (Gln) is known to have immunomodulatory effects in metabolic stressed conditions. This study investigated the effects of post-treatment of alanyl-glutamine (Ala-Gln) on Th cell-associated cytokine expressions and inflammatory reaction in dextran sulfate sodium (DSS)-induced colitis. C57BL/6 mice received distilled water containing 3% DSS for 5days to induce colitis, whereas the normal control (NC) group received distilled water. After induction of colitis, one of the colitis groups (DG) was intraperitoneally injected with an Ala-Gln solution (0.5gGln/kg/d), and the saline DSS group (DS) received an identical volume of saline. After treatment for 3days, mice were sacrificed, and the blood and tissue samples were collected for further analysis. DSS colitis resulted in higher percentages of blood interleukin (IL)-17-secreting Th cells and greater expression of Th cell-associated cytokine messenger RNA (mRNA) in the mesenteric lymph nodes (MLN). Also, luminal immunoglobin (Ig) G, keratinocyte-derived chemokine, and macrophage chemoattractant protein-1 levels were higher in the DS group than the NC group, whereas these parameters did not differ between the DG and NC groups. The DG group had lower blood IL-17A, 17F, MLN IL-17 mRNA and macrophage percentage in the peritoneal lavage fluid than those of the DS group. These results suggest that post-treatment with Ala-Gln suppressed Th17-associated cytokine expressions, reduced macrophage infiltration into the peritoneal cavity and decreased pro-inflammatory cytokine production in the colon, thus may have attenuated inflammatory response in DSS-induced colitis.
•Post-treatment with Ala-Gln attenuated inflammatory response in a model of colitis.•Ala-Gln administration suppressed Th17-associated cytokine production.•Ala-Gln reduced macrophage infiltration and pro-inflammatory cytokine production.</description><subject>Alanyl-glutamine</subject><subject>Animals</subject><subject>Body Weight</subject><subject>Colitis - chemically induced</subject><subject>Colitis - drug therapy</subject><subject>Colon</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Dextran Sulfate - toxicity</subject><subject>Dipeptides - therapeutic use</subject><subject>DSS-colitis</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Immunoglobin G</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - drug therapy</subject><subject>Interleukin-17</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>T helper cells</subject><subject>Th17 Cells - drug effects</subject><subject>Th17 Cells - physiology</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqFkUtv1TAQhS0EoqXwDxDKkk2CH7Edb5CqqjykSmzK2prYE_BV4gTbQdwl_xxfbmEJqxkdnW9GM4eQl4x2jDL15tCFWMKydZwy0VHZUdo_Ipds0EPLNJWPay-VbqVW5oI8y_lAadV79pRccKE5U4O5JD-vZ4jHuf0y7wWWELEBX0vIJUEJa2zyvm0Jc8bc3H9luoHom4R-d1UIcZphWaCs6VhFcL-JEBuPPyp_gucJCjZ59WFf2hBPnG_A7VV06xxKyM_JkwnmjC8e6hX5_O72_uZDe_fp_ceb67vW9YqVVlIundJoxMS5duOkRwMC-4H60U1uBDVBX-_1TvNxGBTA6BUFLgavjFFeXJHX57lbWr_tmItdQnY41_tx3bNlklJtGBX9_63CGCN6Knm19merS2vOCSe7pbBAOlpG7Skne7DnnOwpJ0ulrTlV7NXDhn1c0P-F_gRTDW_PBqwv-R4w2ewCxvq9kNAV69fw7w2_AExSqWw</recordid><startdate>20130901</startdate><enddate>20130901</enddate><creator>Hou, Yu-Chen</creator><creator>Liu, Jun-Jen</creator><creator>Pai, Man-Hui</creator><creator>Tsou, Shung-Sheng</creator><creator>Yeh, Sung-Ling</creator><general>Elsevier 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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20130901</creationdate><title>Alanyl-glutamine administration suppresses Th17 and reduces inflammatory reaction in dextran sulfate sodium-induced acute colitis</title><author>Hou, Yu-Chen ; Liu, Jun-Jen ; Pai, Man-Hui ; Tsou, Shung-Sheng ; Yeh, Sung-Ling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-5025c67e93f227cbf7b9a3e480dbcfcba6fa4567dc72b886aabd60a238d6996d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alanyl-glutamine</topic><topic>Animals</topic><topic>Body Weight</topic><topic>Colitis - chemically induced</topic><topic>Colitis - drug therapy</topic><topic>Colon</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Dextran Sulfate - toxicity</topic><topic>Dipeptides - therapeutic use</topic><topic>DSS-colitis</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Immunoglobin G</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - drug therapy</topic><topic>Interleukin-17</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>T helper cells</topic><topic>Th17 Cells - drug effects</topic><topic>Th17 Cells - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hou, Yu-Chen</creatorcontrib><creatorcontrib>Liu, Jun-Jen</creatorcontrib><creatorcontrib>Pai, Man-Hui</creatorcontrib><creatorcontrib>Tsou, Shung-Sheng</creatorcontrib><creatorcontrib>Yeh, Sung-Ling</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hou, Yu-Chen</au><au>Liu, Jun-Jen</au><au>Pai, Man-Hui</au><au>Tsou, Shung-Sheng</au><au>Yeh, Sung-Ling</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alanyl-glutamine administration suppresses Th17 and reduces inflammatory reaction in dextran sulfate sodium-induced acute colitis</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2013-09-01</date><risdate>2013</risdate><volume>17</volume><issue>1</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>ObjectType-Article-2</notes><notes>ObjectType-Feature-1</notes><abstract>T helper (Th) cells play a major role in the pathogenesis of inflammatory bowel disease (IBD). Glutamine (Gln) is known to have immunomodulatory effects in metabolic stressed conditions. This study investigated the effects of post-treatment of alanyl-glutamine (Ala-Gln) on Th cell-associated cytokine expressions and inflammatory reaction in dextran sulfate sodium (DSS)-induced colitis. C57BL/6 mice received distilled water containing 3% DSS for 5days to induce colitis, whereas the normal control (NC) group received distilled water. After induction of colitis, one of the colitis groups (DG) was intraperitoneally injected with an Ala-Gln solution (0.5gGln/kg/d), and the saline DSS group (DS) received an identical volume of saline. After treatment for 3days, mice were sacrificed, and the blood and tissue samples were collected for further analysis. DSS colitis resulted in higher percentages of blood interleukin (IL)-17-secreting Th cells and greater expression of Th cell-associated cytokine messenger RNA (mRNA) in the mesenteric lymph nodes (MLN). Also, luminal immunoglobin (Ig) G, keratinocyte-derived chemokine, and macrophage chemoattractant protein-1 levels were higher in the DS group than the NC group, whereas these parameters did not differ between the DG and NC groups. The DG group had lower blood IL-17A, 17F, MLN IL-17 mRNA and macrophage percentage in the peritoneal lavage fluid than those of the DS group. These results suggest that post-treatment with Ala-Gln suppressed Th17-associated cytokine expressions, reduced macrophage infiltration into the peritoneal cavity and decreased pro-inflammatory cytokine production in the colon, thus may have attenuated inflammatory response in DSS-induced colitis.
•Post-treatment with Ala-Gln attenuated inflammatory response in a model of colitis.•Ala-Gln administration suppressed Th17-associated cytokine production.•Ala-Gln reduced macrophage infiltration and pro-inflammatory cytokine production.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>23721689</pmid><doi>10.1016/j.intimp.2013.05.004</doi><tpages>8</tpages></addata></record> |
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| subjects | Alanyl-glutamine Animals Body Weight Colitis - chemically induced Colitis - drug therapy Colon Cytokines - genetics Cytokines - metabolism Dextran Sulfate - toxicity Dipeptides - therapeutic use DSS-colitis Gene Expression Regulation - drug effects Immunoglobin G Inflammation - chemically induced Inflammation - drug therapy Interleukin-17 Male Mice Mice, Inbred C57BL RNA, Messenger - genetics RNA, Messenger - metabolism T helper cells Th17 Cells - drug effects Th17 Cells - physiology |
| title | Alanyl-glutamine administration suppresses Th17 and reduces inflammatory reaction in dextran sulfate sodium-induced acute colitis |
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