Roles of TLR2, TLR4, NOD2, and NOD1 in Pulp Fibroblasts
Pulp fibroblasts express various pro-inflammatory mediators leading to marked infiltration of inflammatory cells in the progression of pulpitis. We hypothesized that pulp fibroblasts play roles in the recognition of invaded caries-related bacteria and the subsequent innate immune responses. We found...
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| Veröffentlicht in: | Journal of dental research 2009-08, Vol.88 (8), p.762-767 |
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| container_title | Journal of dental research |
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| creator | Hirao, K. Yumoto, H. Takahashi, K. Mukai, K. Nakanishi, T. Matsuo, T. |
| description | Pulp fibroblasts express various pro-inflammatory mediators leading to marked infiltration of inflammatory cells in the progression of pulpitis. We hypothesized that pulp fibroblasts play roles in the recognition of invaded caries-related bacteria and the subsequent innate immune responses. We found clear expressions of TLR2, NOD1, and NOD2 and a faint expression of TLR4 in human dental pulp fibroblasts (HDPF) by RT-PCR and flow cytometry. We also observed that various pro-inflammatory mediators, including cytokines, chemokines, adhesion molecules, prostaglandin E2 and its key enzyme COX-2, not iNOS or caspase-1, were markedly up-regulated by stimulation with these TLR and NOD agonists. More over, the NOD2 agonist acted synergistically with the TLR2, not the TLR4, agonist to stimulate the production of pro-inflammatory mediators in HDPF. These findings indicate that TLR2, TLR4, NOD2, and NOD1 in HDPF are functional receptors, and NOD2 is a modulator of signals transmitted through TLR2 in pulpal immune responses, leading to progressive pulpitis. |
| doi_str_mv | 10.1177/0022034509341779 |
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We hypothesized that pulp fibroblasts play roles in the recognition of invaded caries-related bacteria and the subsequent innate immune responses. We found clear expressions of TLR2, NOD1, and NOD2 and a faint expression of TLR4 in human dental pulp fibroblasts (HDPF) by RT-PCR and flow cytometry. We also observed that various pro-inflammatory mediators, including cytokines, chemokines, adhesion molecules, prostaglandin E2 and its key enzyme COX-2, not iNOS or caspase-1, were markedly up-regulated by stimulation with these TLR and NOD agonists. More over, the NOD2 agonist acted synergistically with the TLR2, not the TLR4, agonist to stimulate the production of pro-inflammatory mediators in HDPF. These findings indicate that TLR2, TLR4, NOD2, and NOD1 in HDPF are functional receptors, and NOD2 is a modulator of signals transmitted through TLR2 in pulpal immune responses, leading to progressive pulpitis.</description><identifier>ISSN: 0022-0345</identifier><identifier>EISSN: 1544-0591</identifier><identifier>DOI: 10.1177/0022034509341779</identifier><identifier>PMID: 19734466</identifier><identifier>CODEN: JDREAF</identifier><language>eng</language><publisher>United States: SAGE Publications</publisher><subject>Acetylmuramyl-Alanyl-Isoglutamine - pharmacology ; Apoptosis - immunology ; Cells, Cultured ; Chemokine CCL2 - analysis ; Chemokine CXCL10 - analysis ; Cyclooxygenase 2 - immunology ; Dental Pulp - cytology ; Dental Pulp - immunology ; Dentistry ; Diaminopimelic Acid - analogs & derivatives ; Dinoprostone - analysis ; Escherichia coli ; Fibroblasts - immunology ; Humans ; Inflammation Mediators - immunology ; Interleukin-6 - analysis ; Interleukin-8 - analysis ; Lipopeptides - pharmacology ; Lipopolysaccharides - pharmacology ; Nod1 Signaling Adaptor Protein - analysis ; Nod1 Signaling Adaptor Protein - antagonists & inhibitors ; Nod2 Signaling Adaptor Protein - analysis ; Nod2 Signaling Adaptor Protein - antagonists & inhibitors ; Pulpitis - immunology ; Signal Transduction - immunology ; Streptococcus mutans - immunology ; Toll-Like Receptor 2 - analysis ; Toll-Like Receptor 2 - antagonists & inhibitors ; Toll-Like Receptor 4 - analysis ; Toll-Like Receptor 4 - antagonists & inhibitors ; Vascular Cell Adhesion Molecule-1 - analysis</subject><ispartof>Journal of dental research, 2009-08, Vol.88 (8), p.762-767</ispartof><rights>2009 International & American Associations for Dental Research</rights><rights>SAGE Publications © Aug 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-8364ec8f25afb2edce1c05eae93c22b55781636f15621d0fc0891b3fb5bbe5453</citedby><cites>FETCH-LOGICAL-c457t-8364ec8f25afb2edce1c05eae93c22b55781636f15621d0fc0891b3fb5bbe5453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0022034509341779$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0022034509341779$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21800,27903,27904,43600,43601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19734466$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirao, K.</creatorcontrib><creatorcontrib>Yumoto, H.</creatorcontrib><creatorcontrib>Takahashi, K.</creatorcontrib><creatorcontrib>Mukai, K.</creatorcontrib><creatorcontrib>Nakanishi, T.</creatorcontrib><creatorcontrib>Matsuo, T.</creatorcontrib><title>Roles of TLR2, TLR4, NOD2, and NOD1 in Pulp Fibroblasts</title><title>Journal of dental research</title><addtitle>J Dent Res</addtitle><description>Pulp fibroblasts express various pro-inflammatory mediators leading to marked infiltration of inflammatory cells in the progression of pulpitis. We hypothesized that pulp fibroblasts play roles in the recognition of invaded caries-related bacteria and the subsequent innate immune responses. We found clear expressions of TLR2, NOD1, and NOD2 and a faint expression of TLR4 in human dental pulp fibroblasts (HDPF) by RT-PCR and flow cytometry. We also observed that various pro-inflammatory mediators, including cytokines, chemokines, adhesion molecules, prostaglandin E2 and its key enzyme COX-2, not iNOS or caspase-1, were markedly up-regulated by stimulation with these TLR and NOD agonists. More over, the NOD2 agonist acted synergistically with the TLR2, not the TLR4, agonist to stimulate the production of pro-inflammatory mediators in HDPF. These findings indicate that TLR2, TLR4, NOD2, and NOD1 in HDPF are functional receptors, and NOD2 is a modulator of signals transmitted through TLR2 in pulpal immune responses, leading to progressive pulpitis.</description><subject>Acetylmuramyl-Alanyl-Isoglutamine - pharmacology</subject><subject>Apoptosis - immunology</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - analysis</subject><subject>Chemokine CXCL10 - analysis</subject><subject>Cyclooxygenase 2 - immunology</subject><subject>Dental Pulp - cytology</subject><subject>Dental Pulp - immunology</subject><subject>Dentistry</subject><subject>Diaminopimelic Acid - analogs & derivatives</subject><subject>Dinoprostone - analysis</subject><subject>Escherichia coli</subject><subject>Fibroblasts - immunology</subject><subject>Humans</subject><subject>Inflammation Mediators - immunology</subject><subject>Interleukin-6 - analysis</subject><subject>Interleukin-8 - analysis</subject><subject>Lipopeptides - pharmacology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Nod1 Signaling Adaptor Protein - analysis</subject><subject>Nod1 Signaling Adaptor Protein - antagonists & inhibitors</subject><subject>Nod2 Signaling Adaptor Protein - analysis</subject><subject>Nod2 Signaling Adaptor Protein - antagonists & inhibitors</subject><subject>Pulpitis - immunology</subject><subject>Signal Transduction - immunology</subject><subject>Streptococcus mutans - immunology</subject><subject>Toll-Like Receptor 2 - analysis</subject><subject>Toll-Like Receptor 2 - antagonists & inhibitors</subject><subject>Toll-Like Receptor 4 - analysis</subject><subject>Toll-Like Receptor 4 - antagonists & inhibitors</subject><subject>Vascular Cell Adhesion Molecule-1 - analysis</subject><issn>0022-0345</issn><issn>1544-0591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kE1Lw0AQhhdRbK3ePUnw4KnR2e_do7RWhWKl1HPY3exKSprUbHPw35vQQqHgZT6YZ94ZXoRuMTxiLOUTACFAGQdNWdfrMzTEnLEUuMbnaNiP034-QFcxrgGwJopeogHWkjImxBDJZV36mNQhWc2XZNxHNk4-FtOuNlXeVzgpquSzLbfJrLBNbUsTd_EaXQRTRn9zyCP0NXtZTd7S-eL1ffI8Tx3jcpcqKph3KhBugiU-dx474N54TR0hlnOpsKAiYC4IziE4UBpbGiy31nPG6Qg97HW3Tf3T-rjLNkV0vixN5es2ZkIKKoHKDrw_Add121TdbxkBzagiCjoI9pBr6hgbH7JtU2xM85thyHpHs1NHu5W7g25rNz4_Lhws7IB0D0Tz7Y9H_xX8AxOJeFI</recordid><startdate>200908</startdate><enddate>200908</enddate><creator>Hirao, K.</creator><creator>Yumoto, H.</creator><creator>Takahashi, K.</creator><creator>Mukai, K.</creator><creator>Nakanishi, T.</creator><creator>Matsuo, T.</creator><general>SAGE Publications</general><general>SAGE PUBLICATIONS, INC</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>7RQ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>200908</creationdate><title>Roles of TLR2, TLR4, NOD2, and NOD1 in Pulp Fibroblasts</title><author>Hirao, K. ; Yumoto, H. ; Takahashi, K. ; Mukai, K. ; Nakanishi, T. ; Matsuo, T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-8364ec8f25afb2edce1c05eae93c22b55781636f15621d0fc0891b3fb5bbe5453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Acetylmuramyl-Alanyl-Isoglutamine - pharmacology</topic><topic>Apoptosis - immunology</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - analysis</topic><topic>Chemokine CXCL10 - analysis</topic><topic>Cyclooxygenase 2 - immunology</topic><topic>Dental Pulp - cytology</topic><topic>Dental Pulp - immunology</topic><topic>Dentistry</topic><topic>Diaminopimelic Acid - analogs & derivatives</topic><topic>Dinoprostone - analysis</topic><topic>Escherichia coli</topic><topic>Fibroblasts - immunology</topic><topic>Humans</topic><topic>Inflammation Mediators - immunology</topic><topic>Interleukin-6 - analysis</topic><topic>Interleukin-8 - analysis</topic><topic>Lipopeptides - pharmacology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Nod1 Signaling Adaptor Protein - analysis</topic><topic>Nod1 Signaling Adaptor Protein - antagonists & inhibitors</topic><topic>Nod2 Signaling Adaptor Protein - analysis</topic><topic>Nod2 Signaling Adaptor Protein - antagonists & inhibitors</topic><topic>Pulpitis - immunology</topic><topic>Signal Transduction - immunology</topic><topic>Streptococcus mutans - immunology</topic><topic>Toll-Like Receptor 2 - analysis</topic><topic>Toll-Like Receptor 2 - antagonists & inhibitors</topic><topic>Toll-Like Receptor 4 - analysis</topic><topic>Toll-Like Receptor 4 - antagonists & inhibitors</topic><topic>Vascular Cell Adhesion Molecule-1 - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hirao, K.</creatorcontrib><creatorcontrib>Yumoto, H.</creatorcontrib><creatorcontrib>Takahashi, K.</creatorcontrib><creatorcontrib>Mukai, K.</creatorcontrib><creatorcontrib>Nakanishi, T.</creatorcontrib><creatorcontrib>Matsuo, T.</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>Career & Technical Education Database</collection><collection>Nursing & Allied Health Database</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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of dental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hirao, K.</au><au>Yumoto, H.</au><au>Takahashi, K.</au><au>Mukai, K.</au><au>Nakanishi, T.</au><au>Matsuo, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles of TLR2, TLR4, NOD2, and NOD1 in Pulp Fibroblasts</atitle><jtitle>Journal of dental research</jtitle><addtitle>J Dent Res</addtitle><date>2009-08</date><risdate>2009</risdate><volume>88</volume><issue>8</issue><spage>762</spage><epage>767</epage><pages>762-767</pages><issn>0022-0345</issn><eissn>1544-0591</eissn><coden>JDREAF</coden><abstract>Pulp fibroblasts express various pro-inflammatory mediators leading to marked infiltration of inflammatory cells in the progression of pulpitis. We hypothesized that pulp fibroblasts play roles in the recognition of invaded caries-related bacteria and the subsequent innate immune responses. We found clear expressions of TLR2, NOD1, and NOD2 and a faint expression of TLR4 in human dental pulp fibroblasts (HDPF) by RT-PCR and flow cytometry. We also observed that various pro-inflammatory mediators, including cytokines, chemokines, adhesion molecules, prostaglandin E2 and its key enzyme COX-2, not iNOS or caspase-1, were markedly up-regulated by stimulation with these TLR and NOD agonists. More over, the NOD2 agonist acted synergistically with the TLR2, not the TLR4, agonist to stimulate the production of pro-inflammatory mediators in HDPF. These findings indicate that TLR2, TLR4, NOD2, and NOD1 in HDPF are functional receptors, and NOD2 is a modulator of signals transmitted through TLR2 in pulpal immune responses, leading to progressive pulpitis.</abstract><cop>United States</cop><pub>SAGE Publications</pub><pmid>19734466</pmid><doi>10.1177/0022034509341779</doi><tpages>6</tpages></addata></record> |
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| subjects | Acetylmuramyl-Alanyl-Isoglutamine - pharmacology Apoptosis - immunology Cells, Cultured Chemokine CCL2 - analysis Chemokine CXCL10 - analysis Cyclooxygenase 2 - immunology Dental Pulp - cytology Dental Pulp - immunology Dentistry Diaminopimelic Acid - analogs & derivatives Dinoprostone - analysis Escherichia coli Fibroblasts - immunology Humans Inflammation Mediators - immunology Interleukin-6 - analysis Interleukin-8 - analysis Lipopeptides - pharmacology Lipopolysaccharides - pharmacology Nod1 Signaling Adaptor Protein - analysis Nod1 Signaling Adaptor Protein - antagonists & inhibitors Nod2 Signaling Adaptor Protein - analysis Nod2 Signaling Adaptor Protein - antagonists & inhibitors Pulpitis - immunology Signal Transduction - immunology Streptococcus mutans - immunology Toll-Like Receptor 2 - analysis Toll-Like Receptor 2 - antagonists & inhibitors Toll-Like Receptor 4 - analysis Toll-Like Receptor 4 - antagonists & inhibitors Vascular Cell Adhesion Molecule-1 - analysis |
| title | Roles of TLR2, TLR4, NOD2, and NOD1 in Pulp Fibroblasts |
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