Toll-like Receptor 10 in Helicobacter pylori Infection
Innate immunity plays important roles in the primary defense against pathogens, and epidemiological studies have suggested a role for Toll-like receptor 1 (TLR1) in Helicobacter pylori susceptibility. Microarray analysis of gastric biopsy specimens from H. pylori-positive and uninfected subjects sho...
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Veröffentlicht in: | The Journal of infectious diseases 2015-11, Vol.212 (10), p.1666-1676 |
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creator | Nagashima, Hiroyuki Iwatani, Shun Cruz, Modesto Jiménez Abreu, José A. Uchida, Tomohisa Mahachai, Varocha Vilaichone, Ratha-korn Graham, David Y. Yamaoka, Yoshio |
description | Innate immunity plays important roles in the primary defense against pathogens, and epidemiological studies have suggested a role for Toll-like receptor 1 (TLR1) in Helicobacter pylori susceptibility. Microarray analysis of gastric biopsy specimens from H. pylori-positive and uninfected subjects showed that TLR10 messenger RNA (mRNA) levels were upregulated approximately 15-fold in infected subjects; these findings were confirmed by real-time quantitative polymerase chain reaction analysis. Immunohistochemical investigation showed increased TLR10 expression in the gastric epithelial cells of infected individuals. When H. pylori was cocultured with NCI-N87 gastric cells, both TLR10 and TLR2 mRNA levels were upregulated. We compared the ability of TLR combinations to mediate nuclear factor-kB (NF-kB) activation. Compared with other TLR2 subfamily heterodimers, the TLR2/TLR10 heterodimer mediated the greatest NF-kB activation following exposure to heat-killed H. pylori or H. pylori lipopolysaccharide. We conclude that TLR10 is a functional receptor involved in the innate immune response to H. pylori infection and that the TLR2/TLR10 heterodimer functions in H. pylori lipopolysaccharide recognition. |
doi_str_mv | 10.1093/infdis/jiv270 |
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Microarray analysis of gastric biopsy specimens from H. pylori-positive and uninfected subjects showed that TLR10 messenger RNA (mRNA) levels were upregulated approximately 15-fold in infected subjects; these findings were confirmed by real-time quantitative polymerase chain reaction analysis. Immunohistochemical investigation showed increased TLR10 expression in the gastric epithelial cells of infected individuals. When H. pylori was cocultured with NCI-N87 gastric cells, both TLR10 and TLR2 mRNA levels were upregulated. We compared the ability of TLR combinations to mediate nuclear factor-kB (NF-kB) activation. Compared with other TLR2 subfamily heterodimers, the TLR2/TLR10 heterodimer mediated the greatest NF-kB activation following exposure to heat-killed H. pylori or H. pylori lipopolysaccharide. We conclude that TLR10 is a functional receptor involved in the innate immune response to H. pylori infection and that the TLR2/TLR10 heterodimer functions in H. pylori lipopolysaccharide recognition.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1093/infdis/jiv270</identifier><identifier>PMID: 25977263</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Cell Line ; Coculture Techniques ; Epithelial Cells - chemistry ; Gastric Mucosa - pathology ; Gene Expression Profiling ; Helicobacter Infections - immunology ; Helicobacter pylori - immunology ; Humans ; Immunohistochemistry ; Lipopolysaccharides - immunology ; Major and Brief Reports ; Microarray Analysis ; NF-kappa B - analysis ; PATHOGENESIS AND HOST RESPONSE ; Real-Time Polymerase Chain Reaction ; Toll-Like Receptor 10 - genetics ; Toll-Like Receptor 10 - metabolism ; Up-Regulation</subject><ispartof>The Journal of infectious diseases, 2015-11, Vol.212 (10), p.1666-1676</ispartof><rights>Copyright © 2015 Oxford University Press on behalf of the Infectious Diseases Society of America</rights><rights>The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.</rights><rights>The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: . 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-97d586cf015731b5095352640f5090dafaa81d07ad970b4cf27cea0ba6c4b8ed3</citedby><cites>FETCH-LOGICAL-c370t-97d586cf015731b5095352640f5090dafaa81d07ad970b4cf27cea0ba6c4b8ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/43709684$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/43709684$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,780,784,803,885,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25977263$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nagashima, Hiroyuki</creatorcontrib><creatorcontrib>Iwatani, Shun</creatorcontrib><creatorcontrib>Cruz, Modesto</creatorcontrib><creatorcontrib>Jiménez Abreu, José A.</creatorcontrib><creatorcontrib>Uchida, Tomohisa</creatorcontrib><creatorcontrib>Mahachai, Varocha</creatorcontrib><creatorcontrib>Vilaichone, Ratha-korn</creatorcontrib><creatorcontrib>Graham, David Y.</creatorcontrib><creatorcontrib>Yamaoka, Yoshio</creatorcontrib><title>Toll-like Receptor 10 in Helicobacter pylori Infection</title><title>The Journal of infectious diseases</title><addtitle>J Infect Dis</addtitle><description>Innate immunity plays important roles in the primary defense against pathogens, and epidemiological studies have suggested a role for Toll-like receptor 1 (TLR1) in Helicobacter pylori susceptibility. Microarray analysis of gastric biopsy specimens from H. pylori-positive and uninfected subjects showed that TLR10 messenger RNA (mRNA) levels were upregulated approximately 15-fold in infected subjects; these findings were confirmed by real-time quantitative polymerase chain reaction analysis. Immunohistochemical investigation showed increased TLR10 expression in the gastric epithelial cells of infected individuals. When H. pylori was cocultured with NCI-N87 gastric cells, both TLR10 and TLR2 mRNA levels were upregulated. We compared the ability of TLR combinations to mediate nuclear factor-kB (NF-kB) activation. Compared with other TLR2 subfamily heterodimers, the TLR2/TLR10 heterodimer mediated the greatest NF-kB activation following exposure to heat-killed H. pylori or H. pylori lipopolysaccharide. We conclude that TLR10 is a functional receptor involved in the innate immune response to H. pylori infection and that the TLR2/TLR10 heterodimer functions in H. pylori lipopolysaccharide recognition.</description><subject>Cell Line</subject><subject>Coculture Techniques</subject><subject>Epithelial Cells - chemistry</subject><subject>Gastric Mucosa - pathology</subject><subject>Gene Expression Profiling</subject><subject>Helicobacter Infections - immunology</subject><subject>Helicobacter pylori - immunology</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Lipopolysaccharides - immunology</subject><subject>Major and Brief Reports</subject><subject>Microarray Analysis</subject><subject>NF-kappa B - analysis</subject><subject>PATHOGENESIS AND HOST RESPONSE</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Toll-Like Receptor 10 - genetics</subject><subject>Toll-Like Receptor 10 - metabolism</subject><subject>Up-Regulation</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkMFLwzAUh4Mobk6PHpUevdS9JG3SXAQZ6oSBIPMc0jTVzKypSTfYf2-lc-jpPXgfv9_jQ-gSwy0GQae2qSsbpyu7JRyO0BjnlKeMYXqMxgCEpLgQYoTOYlwBQEYZP0UjkgvOCaNjxJbeudTZT5O8Gm3azocEQ2KbZG6c1b5UujMhaXfOB5s8N7XRnfXNOTqplYvmYj8n6O3xYTmbp4uXp-fZ_SLVlEOXCl7lBdM14JxTXOYgcpoTlkHdr1CpWqkCV8BVJTiUma4J10ZBqZjOysJUdILuhtx2U65NpU3TBeVkG-xahZ30ysr_l8Z-yHe_lRkjmGSiD7jZBwT_tTGxk2sbtXFONcZvosSccCFyKLIeTQdUBx9jMPWhBoP8cS0H13Jw3fPXf3870L9ye-BqAFax13q4Z70awfrCb-fPhmw</recordid><startdate>20151115</startdate><enddate>20151115</enddate><creator>Nagashima, Hiroyuki</creator><creator>Iwatani, Shun</creator><creator>Cruz, Modesto</creator><creator>Jiménez Abreu, José A.</creator><creator>Uchida, Tomohisa</creator><creator>Mahachai, Varocha</creator><creator>Vilaichone, Ratha-korn</creator><creator>Graham, David Y.</creator><creator>Yamaoka, Yoshio</creator><general>Oxford University Press</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>5PM</scope></search><sort><creationdate>20151115</creationdate><title>Toll-like Receptor 10 in Helicobacter pylori Infection</title><author>Nagashima, Hiroyuki ; Iwatani, Shun ; Cruz, Modesto ; Jiménez Abreu, José A. ; Uchida, Tomohisa ; Mahachai, Varocha ; Vilaichone, Ratha-korn ; Graham, David Y. ; Yamaoka, Yoshio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-97d586cf015731b5095352640f5090dafaa81d07ad970b4cf27cea0ba6c4b8ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Cell Line</topic><topic>Coculture Techniques</topic><topic>Epithelial Cells - chemistry</topic><topic>Gastric Mucosa - pathology</topic><topic>Gene Expression Profiling</topic><topic>Helicobacter Infections - immunology</topic><topic>Helicobacter pylori - immunology</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Lipopolysaccharides - immunology</topic><topic>Major and Brief Reports</topic><topic>Microarray Analysis</topic><topic>NF-kappa B - analysis</topic><topic>PATHOGENESIS AND HOST RESPONSE</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Toll-Like Receptor 10 - genetics</topic><topic>Toll-Like Receptor 10 - metabolism</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nagashima, Hiroyuki</creatorcontrib><creatorcontrib>Iwatani, Shun</creatorcontrib><creatorcontrib>Cruz, Modesto</creatorcontrib><creatorcontrib>Jiménez Abreu, José A.</creatorcontrib><creatorcontrib>Uchida, Tomohisa</creatorcontrib><creatorcontrib>Mahachai, Varocha</creatorcontrib><creatorcontrib>Vilaichone, Ratha-korn</creatorcontrib><creatorcontrib>Graham, David Y.</creatorcontrib><creatorcontrib>Yamaoka, Yoshio</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>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nagashima, Hiroyuki</au><au>Iwatani, Shun</au><au>Cruz, Modesto</au><au>Jiménez Abreu, José A.</au><au>Uchida, Tomohisa</au><au>Mahachai, Varocha</au><au>Vilaichone, Ratha-korn</au><au>Graham, David Y.</au><au>Yamaoka, Yoshio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Toll-like Receptor 10 in Helicobacter pylori Infection</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>2015-11-15</date><risdate>2015</risdate><volume>212</volume><issue>10</issue><spage>1666</spage><epage>1676</epage><pages>1666-1676</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><abstract>Innate immunity plays important roles in the primary defense against pathogens, and epidemiological studies have suggested a role for Toll-like receptor 1 (TLR1) in Helicobacter pylori susceptibility. Microarray analysis of gastric biopsy specimens from H. pylori-positive and uninfected subjects showed that TLR10 messenger RNA (mRNA) levels were upregulated approximately 15-fold in infected subjects; these findings were confirmed by real-time quantitative polymerase chain reaction analysis. Immunohistochemical investigation showed increased TLR10 expression in the gastric epithelial cells of infected individuals. When H. pylori was cocultured with NCI-N87 gastric cells, both TLR10 and TLR2 mRNA levels were upregulated. We compared the ability of TLR combinations to mediate nuclear factor-kB (NF-kB) activation. Compared with other TLR2 subfamily heterodimers, the TLR2/TLR10 heterodimer mediated the greatest NF-kB activation following exposure to heat-killed H. pylori or H. pylori lipopolysaccharide. We conclude that TLR10 is a functional receptor involved in the innate immune response to H. pylori infection and that the TLR2/TLR10 heterodimer functions in H. pylori lipopolysaccharide recognition.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>25977263</pmid><doi>10.1093/infdis/jiv270</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Cell Line Coculture Techniques Epithelial Cells - chemistry Gastric Mucosa - pathology Gene Expression Profiling Helicobacter Infections - immunology Helicobacter pylori - immunology Humans Immunohistochemistry Lipopolysaccharides - immunology Major and Brief Reports Microarray Analysis NF-kappa B - analysis PATHOGENESIS AND HOST RESPONSE Real-Time Polymerase Chain Reaction Toll-Like Receptor 10 - genetics Toll-Like Receptor 10 - metabolism Up-Regulation |
title | Toll-like Receptor 10 in Helicobacter pylori Infection |
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