Choline Deficiency Causes Colonic Type II Natural Killer T (NKT) Cell Loss and Alleviates Murine Colitis under Type I NKT Cell Deficiency
Serum levels of choline and its derivatives are lower in patients with inflammatory bowel disease (IBD) than in healthy individuals. However, the effect of choline deficiency on the severity of colitis has not been investigated. In the present study, we investigated the role of choline deficiency in...
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description | Serum levels of choline and its derivatives are lower in patients with inflammatory bowel disease (IBD) than in healthy individuals. However, the effect of choline deficiency on the severity of colitis has not been investigated. In the present study, we investigated the role of choline deficiency in dextran sulfate sodium (DSS)-induced colitis in mice. Methionine-choline-deficient (MCD) diet lowered the levels of type II natural killer T (NKT) cells in the colonic lamina propria, peritoneal cavity, and mesenteric lymph nodes, and increased the levels of type II NKT cells in the livers of wild-type B6 mice compared with that in mice fed a control (CTR) diet. The gene expression pattern of the chemokine receptor CXCR6, which promotes NKT cell accumulation, varied between colon and liver in a manner dependent on the changes in the type II NKT cell levels. To examine the role of type II NKT cells in colitis under choline-deficient conditions, we assessed the severity of DSS-induced colitis in type I NKT cell-deficient (Jα18-/-) or type I and type II NKT cell-deficient (CD1d-/-) mice fed the MCD or CTR diets. The MCD diet led to amelioration of inflammation, decreases in interferon (IFN)-γ and interleukin (IL)-4 secretion, and a decrease in the number of IFN-γ and IL-4-producing NKT cells in Jα18-/- mice but not in CD1d-/- mice. Finally, adaptive transfer of lymphocytes with type II NKT cells exacerbated DSS-induced colitis in Jα18-/- mice with MCD diet. These results suggest that choline deficiency causes proinflammatory type II NKT cell loss and alleviates DSS-induced colitis. Thus, inflammation in DSS-induced colitis under choline deficiency is caused by type II NKT cell-dependent mechanisms, including decreased type II NKT cell and proinflammatory cytokine levels. |
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However, the effect of choline deficiency on the severity of colitis has not been investigated. In the present study, we investigated the role of choline deficiency in dextran sulfate sodium (DSS)-induced colitis in mice. Methionine-choline-deficient (MCD) diet lowered the levels of type II natural killer T (NKT) cells in the colonic lamina propria, peritoneal cavity, and mesenteric lymph nodes, and increased the levels of type II NKT cells in the livers of wild-type B6 mice compared with that in mice fed a control (CTR) diet. The gene expression pattern of the chemokine receptor CXCR6, which promotes NKT cell accumulation, varied between colon and liver in a manner dependent on the changes in the type II NKT cell levels. To examine the role of type II NKT cells in colitis under choline-deficient conditions, we assessed the severity of DSS-induced colitis in type I NKT cell-deficient (Jα18-/-) or type I and type II NKT cell-deficient (CD1d-/-) mice fed the MCD or CTR diets. The MCD diet led to amelioration of inflammation, decreases in interferon (IFN)-γ and interleukin (IL)-4 secretion, and a decrease in the number of IFN-γ and IL-4-producing NKT cells in Jα18-/- mice but not in CD1d-/- mice. Finally, adaptive transfer of lymphocytes with type II NKT cells exacerbated DSS-induced colitis in Jα18-/- mice with MCD diet. These results suggest that choline deficiency causes proinflammatory type II NKT cell loss and alleviates DSS-induced colitis. Thus, inflammation in DSS-induced colitis under choline deficiency is caused by type II NKT cell-dependent mechanisms, including decreased type II NKT cell and proinflammatory cytokine levels.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0169681</identifier><identifier>PMID: 28095507</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Biological response modifiers ; Biology and Life Sciences ; CD1d antigen ; Chemokines ; Choline ; Choline Deficiency - complications ; Colitis ; Colitis - chemically induced ; Colitis - immunology ; Colitis - prevention & control ; Colon ; Cytokines - metabolism ; Dextran ; Dextran sulfate ; Dextran Sulfate - toxicity ; Diet ; Disease Models, Animal ; Ecology and Environmental Sciences ; Endoscopy ; Gastroenterology ; Gene expression ; Health aspects ; Health sciences ; Hepatology ; Hospitals ; Immunology ; Inflammation - etiology ; Inflammation - prevention & control ; Inflammatory bowel disease ; Inflammatory bowel diseases ; Interferon ; Interferon-gamma - metabolism ; Interleukin 4 ; Intestine ; Laboratory animals ; Lamina propria ; Life sciences ; Liver ; Liver diseases ; Lymph nodes ; Lymphocytes ; Lymphocytes T ; Male ; Medicine and Health Sciences ; Metabolism ; Methionine ; Mice ; Mice, Inbred C57BL ; Natural killer cells ; Natural Killer T-Cells - immunology ; Nutrition research ; Pathogens ; Peritoneum ; Physical Sciences ; Physiology ; Research and Analysis Methods ; Risk factors ; Rodents ; Serum levels ; Sodium ; Sulfates ; Surgery ; T cell receptors ; γ-Interferon</subject><ispartof>PloS one, 2017, Vol.12 (1), p.e0169681-e0169681</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Sagami et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Sagami et al 2017 Sagami et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c556t-c9291c9178f5db4dd1b3a18011ee245ebb0fb87a8f3b36321f00d4bef49d0ed13</citedby><cites>FETCH-LOGICAL-c556t-c9291c9178f5db4dd1b3a18011ee245ebb0fb87a8f3b36321f00d4bef49d0ed13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5241147/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5241147/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,4010,23845,27900,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28095507$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sagami, Shintaro</creatorcontrib><creatorcontrib>Ueno, Yoshitaka</creatorcontrib><creatorcontrib>Tanaka, Shinji</creatorcontrib><creatorcontrib>Fujita, Akira</creatorcontrib><creatorcontrib>Niitsu, Hiroaki</creatorcontrib><creatorcontrib>Hayashi, Ryohei</creatorcontrib><creatorcontrib>Hyogo, Hideyuki</creatorcontrib><creatorcontrib>Hinoi, Takao</creatorcontrib><creatorcontrib>Kitadai, Yasuhiko</creatorcontrib><creatorcontrib>Chayama, Kazuaki</creatorcontrib><title>Choline Deficiency Causes Colonic Type II Natural Killer T (NKT) Cell Loss and Alleviates Murine Colitis under Type I NKT Cell Deficiency</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Serum levels of choline and its derivatives are lower in patients with inflammatory bowel disease (IBD) than in healthy individuals. However, the effect of choline deficiency on the severity of colitis has not been investigated. In the present study, we investigated the role of choline deficiency in dextran sulfate sodium (DSS)-induced colitis in mice. Methionine-choline-deficient (MCD) diet lowered the levels of type II natural killer T (NKT) cells in the colonic lamina propria, peritoneal cavity, and mesenteric lymph nodes, and increased the levels of type II NKT cells in the livers of wild-type B6 mice compared with that in mice fed a control (CTR) diet. The gene expression pattern of the chemokine receptor CXCR6, which promotes NKT cell accumulation, varied between colon and liver in a manner dependent on the changes in the type II NKT cell levels. To examine the role of type II NKT cells in colitis under choline-deficient conditions, we assessed the severity of DSS-induced colitis in type I NKT cell-deficient (Jα18-/-) or type I and type II NKT cell-deficient (CD1d-/-) mice fed the MCD or CTR diets. The MCD diet led to amelioration of inflammation, decreases in interferon (IFN)-γ and interleukin (IL)-4 secretion, and a decrease in the number of IFN-γ and IL-4-producing NKT cells in Jα18-/- mice but not in CD1d-/- mice. Finally, adaptive transfer of lymphocytes with type II NKT cells exacerbated DSS-induced colitis in Jα18-/- mice with MCD diet. These results suggest that choline deficiency causes proinflammatory type II NKT cell loss and alleviates DSS-induced colitis. Thus, inflammation in DSS-induced colitis under choline deficiency is caused by type II NKT cell-dependent mechanisms, including decreased type II NKT cell and proinflammatory cytokine levels.</description><subject>Analysis</subject><subject>Animals</subject><subject>Biological response modifiers</subject><subject>Biology and Life Sciences</subject><subject>CD1d antigen</subject><subject>Chemokines</subject><subject>Choline</subject><subject>Choline Deficiency - complications</subject><subject>Colitis</subject><subject>Colitis - chemically induced</subject><subject>Colitis - immunology</subject><subject>Colitis - prevention & control</subject><subject>Colon</subject><subject>Cytokines - metabolism</subject><subject>Dextran</subject><subject>Dextran sulfate</subject><subject>Dextran Sulfate - toxicity</subject><subject>Diet</subject><subject>Disease Models, Animal</subject><subject>Ecology and Environmental 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Sciences</subject><subject>Metabolism</subject><subject>Methionine</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Natural killer cells</subject><subject>Natural Killer T-Cells - immunology</subject><subject>Nutrition research</subject><subject>Pathogens</subject><subject>Peritoneum</subject><subject>Physical Sciences</subject><subject>Physiology</subject><subject>Research and Analysis Methods</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Serum levels</subject><subject>Sodium</subject><subject>Sulfates</subject><subject>Surgery</subject><subject>T cell 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Akira</au><au>Niitsu, Hiroaki</au><au>Hayashi, Ryohei</au><au>Hyogo, Hideyuki</au><au>Hinoi, Takao</au><au>Kitadai, Yasuhiko</au><au>Chayama, Kazuaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Choline Deficiency Causes Colonic Type II Natural Killer T (NKT) Cell Loss and Alleviates Murine Colitis under Type I NKT Cell Deficiency</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017</date><risdate>2017</risdate><volume>12</volume><issue>1</issue><spage>e0169681</spage><epage>e0169681</epage><pages>e0169681-e0169681</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Serum levels of choline and its derivatives are lower in patients with inflammatory bowel disease (IBD) than in healthy individuals. However, the effect of choline deficiency on the severity of colitis has not been investigated. In the present study, we investigated the role of choline deficiency in dextran sulfate sodium (DSS)-induced colitis in mice. Methionine-choline-deficient (MCD) diet lowered the levels of type II natural killer T (NKT) cells in the colonic lamina propria, peritoneal cavity, and mesenteric lymph nodes, and increased the levels of type II NKT cells in the livers of wild-type B6 mice compared with that in mice fed a control (CTR) diet. The gene expression pattern of the chemokine receptor CXCR6, which promotes NKT cell accumulation, varied between colon and liver in a manner dependent on the changes in the type II NKT cell levels. To examine the role of type II NKT cells in colitis under choline-deficient conditions, we assessed the severity of DSS-induced colitis in type I NKT cell-deficient (Jα18-/-) or type I and type II NKT cell-deficient (CD1d-/-) mice fed the MCD or CTR diets. The MCD diet led to amelioration of inflammation, decreases in interferon (IFN)-γ and interleukin (IL)-4 secretion, and a decrease in the number of IFN-γ and IL-4-producing NKT cells in Jα18-/- mice but not in CD1d-/- mice. Finally, adaptive transfer of lymphocytes with type II NKT cells exacerbated DSS-induced colitis in Jα18-/- mice with MCD diet. These results suggest that choline deficiency causes proinflammatory type II NKT cell loss and alleviates DSS-induced colitis. Thus, inflammation in DSS-induced colitis under choline deficiency is caused by type II NKT cell-dependent mechanisms, including decreased type II NKT cell and proinflammatory cytokine levels.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28095507</pmid><doi>10.1371/journal.pone.0169681</doi><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2017, Vol.12 (1), p.e0169681-e0169681 |
issn | 1932-6203 1932-6203 |
language | eng |
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source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
subjects | Analysis Animals Biological response modifiers Biology and Life Sciences CD1d antigen Chemokines Choline Choline Deficiency - complications Colitis Colitis - chemically induced Colitis - immunology Colitis - prevention & control Colon Cytokines - metabolism Dextran Dextran sulfate Dextran Sulfate - toxicity Diet Disease Models, Animal Ecology and Environmental Sciences Endoscopy Gastroenterology Gene expression Health aspects Health sciences Hepatology Hospitals Immunology Inflammation - etiology Inflammation - prevention & control Inflammatory bowel disease Inflammatory bowel diseases Interferon Interferon-gamma - metabolism Interleukin 4 Intestine Laboratory animals Lamina propria Life sciences Liver Liver diseases Lymph nodes Lymphocytes Lymphocytes T Male Medicine and Health Sciences Metabolism Methionine Mice Mice, Inbred C57BL Natural killer cells Natural Killer T-Cells - immunology Nutrition research Pathogens Peritoneum Physical Sciences Physiology Research and Analysis Methods Risk factors Rodents Serum levels Sodium Sulfates Surgery T cell receptors γ-Interferon |
title | Choline Deficiency Causes Colonic Type II Natural Killer T (NKT) Cell Loss and Alleviates Murine Colitis under Type I NKT Cell Deficiency |
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