TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo
Toll-like receptors (TLRs) 2 and 4 play critical roles in intestinal inflammation caused by Fusobacterium nucleatum (F. nucleatum) infection, but the role of TLR2/TLR4 in regulation of proinflammatory cytokines remains unknown. In this study, through microarray analysis and qRT-PCR, we showed that T...
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| description | Toll-like receptors (TLRs) 2 and 4 play critical roles in intestinal inflammation caused by Fusobacterium nucleatum (F. nucleatum) infection, but the role of TLR2/TLR4 in regulation of proinflammatory cytokines remains unknown. In this study, through microarray analysis and qRT-PCR, we showed that TLR2/TLR4 are involved in the F. nucleatum-induced inflammatory signaling pathway in Caco-2 cells, C57BL/6 mice and human clinical specimens. In TLR2-/- and TLR4-/- mice, F. nucleatum infection resulted in increased colonization of the bacteria and production of the proinflammatory cytokines IL-8, IL-1β and TNF-α. In addition, the ratio of Foxp3+ CD4+ T cells in the total CD4+ T cells in TLR2-/- and TLR4-/- mice was less than that in wild-type mice, and the ratio in hybrid mice was more than that in knockout mice, which suggested that TLR2/TLR4 mediated the number of Tregs. Furthermore, it was observed that inflammatory cytokine levels were reduced in TLR2-/- mice after Treg transfer. Thus, these data indicate that TLR2/TLR4 regulate F. nucleatum-induced inflammatory cytokines through Tregs in vivo. |
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In this study, through microarray analysis and qRT-PCR, we showed that TLR2/TLR4 are involved in the F. nucleatum-induced inflammatory signaling pathway in Caco-2 cells, C57BL/6 mice and human clinical specimens. In TLR2-/- and TLR4-/- mice, F. nucleatum infection resulted in increased colonization of the bacteria and production of the proinflammatory cytokines IL-8, IL-1β and TNF-α. In addition, the ratio of Foxp3+ CD4+ T cells in the total CD4+ T cells in TLR2-/- and TLR4-/- mice was less than that in wild-type mice, and the ratio in hybrid mice was more than that in knockout mice, which suggested that TLR2/TLR4 mediated the number of Tregs. Furthermore, it was observed that inflammatory cytokine levels were reduced in TLR2-/- mice after Treg transfer. Thus, these data indicate that TLR2/TLR4 regulate F. nucleatum-induced inflammatory cytokines through Tregs in vivo.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0186179</identifier><identifier>PMID: 29016688</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Analysis ; Animals ; Autophagy ; Bacteria ; Biology and Life Sciences ; Caco-2 Cells ; CD4 antigen ; Colonization ; Colorectal cancer ; Cytokines ; Data transfer (computers) ; Female ; Foxp3 protein ; Fusobacterium Infections - immunology ; Fusobacterium Infections - microbiology ; Fusobacterium Infections - pathology ; Fusobacterium nucleatum ; Fusobacterium nucleatum - immunology ; Fusobacterium nucleatum - pathogenicity ; Gram-negative bacteria ; Humans ; Immune system ; Immunology ; Infections ; Inflammation ; Inflammation - genetics ; Inflammation - immunology ; Inflammation - microbiology ; Inflammatory bowel disease ; Interleukin 1 ; Interleukin 8 ; Intestine ; Intestines - microbiology ; Intestines - pathology ; Lymphocytes ; Lymphocytes T ; Male ; Medical laboratories ; Medicine and Health Sciences ; Mice ; Mice, Knockout ; Microarray Analysis ; Middle Aged ; Orthodontics ; Periodontal diseases ; Proteins ; Receptors ; Research and Analysis Methods ; Risk factors ; Signal Transduction ; Studies ; T-Lymphocytes, Regulatory - immunology ; TLR2 protein ; TLR4 protein ; Toll-Like Receptor 2 - genetics ; Toll-Like Receptor 2 - immunology ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - immunology ; Toll-like receptors ; Tumor necrosis factor</subject><ispartof>PloS one, 2017-10, Vol.12 (10), p.e0186179-e0186179</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Jia 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. 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In this study, through microarray analysis and qRT-PCR, we showed that TLR2/TLR4 are involved in the F. nucleatum-induced inflammatory signaling pathway in Caco-2 cells, C57BL/6 mice and human clinical specimens. In TLR2-/- and TLR4-/- mice, F. nucleatum infection resulted in increased colonization of the bacteria and production of the proinflammatory cytokines IL-8, IL-1β and TNF-α. In addition, the ratio of Foxp3+ CD4+ T cells in the total CD4+ T cells in TLR2-/- and TLR4-/- mice was less than that in wild-type mice, and the ratio in hybrid mice was more than that in knockout mice, which suggested that TLR2/TLR4 mediated the number of Tregs. Furthermore, it was observed that inflammatory cytokine levels were reduced in TLR2-/- mice after Treg transfer. 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genetics</subject><subject>Toll-Like Receptor 2 - immunology</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11r2zAUhs3YWLts_2BshsHYLpJK1oelm0Ep6xYIFLpst-JYlhMF20olO6z_fvLilnj0Yhjsw_Hzvkc60kmStxgtMMnxxc71voV6sXetWSAsOM7ls-QcS5LNeYbI85P4LHkVwg4hRgTnL5OzTCLMuRDnSVivbrOL-KIp6M4eoLOuTW1b9tqEdO3NJqTQlmno93tvQohJ23YmdDbWjmFVQ9McRRr6YMq0uE-v--CKaGe87Zu07XVtoIuRbdODPbjXyYsK6mDejN9Z8vP66_rq-3x18215dbma65yJbq4pw0xSLCRBAgRnkAMHgwkVjFaiqoBpU1SQFwTRqiiMNLTgMmNECyIiN0veH333tQtq7FdQWFKJOBm6MUuWR6J0sFN7bxvw98qBVX8Tzm8U-M7G9SssdF4WmhMR9TnDghVaFhgyTPNSYoheX8ZqfdGYUpu281BPTKd_WrtVG3dQjBOCuYgGn0YD7-762GLV2KBNXUNrXD-smyGc50TQiH74B316dyO1gbiBeFYu1tWDqbpkSOSCUIIitXiCik9pGqvj5apszE8EnyeCyHTmd7eJxx_U8sft_7M3v6bsxxN2a6DutsHV_XC5whSkR1B7F4I31WOTMVLDbDx0Qw2zocbZiLJ3pwf0KHoYBvIHbKwKAA</recordid><startdate>20171009</startdate><enddate>20171009</enddate><creator>Jia, Yin-Ping</creator><creator>Wang, Kun</creator><creator>Zhang, Zhu-Jun</creator><creator>Tong, Ya-Nan</creator><creator>Han, Dan</creator><creator>Hu, Chun-Yu</creator><creator>Li, Qian</creator><creator>Xiang, Yang</creator><creator>Mao, Xu-Hu</creator><creator>Tang, Bin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-1762-3883</orcidid></search><sort><creationdate>20171009</creationdate><title>TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo</title><author>Jia, Yin-Ping ; Wang, Kun ; Zhang, Zhu-Jun ; Tong, Ya-Nan ; Han, Dan ; Hu, Chun-Yu ; Li, Qian ; Xiang, Yang ; Mao, Xu-Hu ; Tang, Bin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-c451594189308a865a7a6ae134854f8ffa5cebfa7b304fbbe9e4b69253c838e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Analysis</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Bacteria</topic><topic>Biology and Life Sciences</topic><topic>Caco-2 Cells</topic><topic>CD4 antigen</topic><topic>Colonization</topic><topic>Colorectal cancer</topic><topic>Cytokines</topic><topic>Data transfer (computers)</topic><topic>Female</topic><topic>Foxp3 protein</topic><topic>Fusobacterium Infections - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jia, Yin-Ping</au><au>Wang, Kun</au><au>Zhang, Zhu-Jun</au><au>Tong, Ya-Nan</au><au>Han, Dan</au><au>Hu, Chun-Yu</au><au>Li, Qian</au><au>Xiang, Yang</au><au>Mao, Xu-Hu</au><au>Tang, Bin</au><au>Chamaillard, Mathias</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-10-09</date><risdate>2017</risdate><volume>12</volume><issue>10</issue><spage>e0186179</spage><epage>e0186179</epage><pages>e0186179-e0186179</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Toll-like receptors (TLRs) 2 and 4 play critical roles in intestinal inflammation caused by Fusobacterium nucleatum (F. nucleatum) infection, but the role of TLR2/TLR4 in regulation of proinflammatory cytokines remains unknown. In this study, through microarray analysis and qRT-PCR, we showed that TLR2/TLR4 are involved in the F. nucleatum-induced inflammatory signaling pathway in Caco-2 cells, C57BL/6 mice and human clinical specimens. In TLR2-/- and TLR4-/- mice, F. nucleatum infection resulted in increased colonization of the bacteria and production of the proinflammatory cytokines IL-8, IL-1β and TNF-α. In addition, the ratio of Foxp3+ CD4+ T cells in the total CD4+ T cells in TLR2-/- and TLR4-/- mice was less than that in wild-type mice, and the ratio in hybrid mice was more than that in knockout mice, which suggested that TLR2/TLR4 mediated the number of Tregs. Furthermore, it was observed that inflammatory cytokine levels were reduced in TLR2-/- mice after Treg transfer. Thus, these data indicate that TLR2/TLR4 regulate F. nucleatum-induced inflammatory cytokines through Tregs in vivo.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29016688</pmid><doi>10.1371/journal.pone.0186179</doi><tpages>e0186179</tpages><orcidid>https://orcid.org/0000-0002-1762-3883</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1949063005 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adult Analysis Animals Autophagy Bacteria Biology and Life Sciences Caco-2 Cells CD4 antigen Colonization Colorectal cancer Cytokines Data transfer (computers) Female Foxp3 protein Fusobacterium Infections - immunology Fusobacterium Infections - microbiology Fusobacterium Infections - pathology Fusobacterium nucleatum Fusobacterium nucleatum - immunology Fusobacterium nucleatum - pathogenicity Gram-negative bacteria Humans Immune system Immunology Infections Inflammation Inflammation - genetics Inflammation - immunology Inflammation - microbiology Inflammatory bowel disease Interleukin 1 Interleukin 8 Intestine Intestines - microbiology Intestines - pathology Lymphocytes Lymphocytes T Male Medical laboratories Medicine and Health Sciences Mice Mice, Knockout Microarray Analysis Middle Aged Orthodontics Periodontal diseases Proteins Receptors Research and Analysis Methods Risk factors Signal Transduction Studies T-Lymphocytes, Regulatory - immunology TLR2 protein TLR4 protein Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - immunology Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - immunology Toll-like receptors Tumor necrosis factor |
| title | TLR2/TLR4 activation induces Tregs and suppresses intestinal inflammation caused by Fusobacterium nucleatum in vivo |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T06%3A45%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TLR2/TLR4%20activation%20induces%20Tregs%20and%20suppresses%20intestinal%20inflammation%20caused%20by%20Fusobacterium%20nucleatum%20in%20vivo&rft.jtitle=PloS%20one&rft.au=Jia,%20Yin-Ping&rft.date=2017-10-09&rft.volume=12&rft.issue=10&rft.spage=e0186179&rft.epage=e0186179&rft.pages=e0186179-e0186179&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0186179&rft_dat=%3Cgale_plos_%3EA508783430%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1949063005&rft_id=info:pmid/29016688&rft_galeid=A508783430&rft_doaj_id=oai_doaj_org_article_18c7dbc63819475185bc9b1a2147d91a&rfr_iscdi=true |