Oral Administration of All‐Trans Retinoic Acid Suppresses Experimental Periodontitis by Modulating the Th17/Treg Imbalance
Background: A T‐helper 17 (Th17)/regulatory T (Treg) imbalance has been suggested recently to play a role in the development of periodontitis. All‐trans retinoic acid (ATRA) has been reported to modulate Th17/Treg imbalances in some diseases. However, the effect of ATRA on periodontitis remains unkn...
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| Veröffentlicht in: | Journal of periodontology (1970) 2014-05, Vol.85 (5), p.740-750 |
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| creator | Wang, Linyuan Wang, Jinyan Jin, Ying Gao, Hong Lin, Xiaoping |
| description | Background: A T‐helper 17 (Th17)/regulatory T (Treg) imbalance has been suggested recently to play a role in the development of periodontitis. All‐trans retinoic acid (ATRA) has been reported to modulate Th17/Treg imbalances in some diseases. However, the effect of ATRA on periodontitis remains unknown. This study observes the effect of ATRA on Th17/Treg imbalance modulation in experimental periodontitis.
Methods: Experimental periodontitis was induced in mice by oral infection with Porphyromonas gingivalis (P. gingivalis). ATRA was orally administered every other day. Alveolar bone resorption (ABR) was estimated by measuring the distance from the cemento‐enamel junction to the alveolar bone crest. CD4+ T‐cell subsets in the cervical lymph nodes (CLNs) and spleen were analyzed by flow cytometry. Th17/Treg cell–related cytokine messenger ribonucleic acid expression was quantified by real‐time reverse transcription‐polymerase chain reaction.
Results: The present data shows that ATRA suppressed ABR and inhibited inflammatory cell infiltration into periodontal tissues. These effects were closely associated with reduced CD4+ retinoid‐related orphan receptor γτ+ cells and increased CD4+ forkhead box P3+ cells in the CLNs. Furthermore, ATRA downregulated interleukin (IL)‐17A expression and upregulated IL‐10 and transforming growth factor‐β1 expression in both the CLNs and P. gingivalis–infected gingival tissues.
Conclusions: These results suggest that ATRA modulation of the Th17/Treg imbalance provides protection against periodontitis by enhancing Treg cell activation and inhibiting Th17 cell activation. These results indicate the potential for clinical prevention of periodontitis. |
| doi_str_mv | 10.1902/jop.2013.130132 |
| format | Article |
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Methods: Experimental periodontitis was induced in mice by oral infection with Porphyromonas gingivalis (P. gingivalis). ATRA was orally administered every other day. Alveolar bone resorption (ABR) was estimated by measuring the distance from the cemento‐enamel junction to the alveolar bone crest. CD4+ T‐cell subsets in the cervical lymph nodes (CLNs) and spleen were analyzed by flow cytometry. Th17/Treg cell–related cytokine messenger ribonucleic acid expression was quantified by real‐time reverse transcription‐polymerase chain reaction.
Results: The present data shows that ATRA suppressed ABR and inhibited inflammatory cell infiltration into periodontal tissues. These effects were closely associated with reduced CD4+ retinoid‐related orphan receptor γτ+ cells and increased CD4+ forkhead box P3+ cells in the CLNs. Furthermore, ATRA downregulated interleukin (IL)‐17A expression and upregulated IL‐10 and transforming growth factor‐β1 expression in both the CLNs and P. gingivalis–infected gingival tissues.
Conclusions: These results suggest that ATRA modulation of the Th17/Treg imbalance provides protection against periodontitis by enhancing Treg cell activation and inhibiting Th17 cell activation. These results indicate the potential for clinical prevention of periodontitis.</description><identifier>ISSN: 0022-3492</identifier><identifier>EISSN: 1943-3670</identifier><identifier>DOI: 10.1902/jop.2013.130132</identifier><identifier>PMID: 23952076</identifier><language>eng</language><publisher>United States: American Academy of Periodontology</publisher><subject>Administration, Oral ; Alveolar Bone Loss - immunology ; Alveolar Bone Loss - microbiology ; Alveolar Bone Loss - prevention & control ; Animals ; Anti-Inflammatory Agents - administration & dosage ; Anti-Inflammatory Agents - therapeutic use ; Bone resorption ; CD4-Positive T-Lymphocytes - drug effects ; Dentistry ; Disease Models, Animal ; Female ; Forkhead Transcription Factors - drug effects ; Interleukin-10 - analysis ; Interleukin-17 - analysis ; Lymph Nodes - pathology ; Lymphocyte Activation - drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Nuclear Receptor Subfamily 1, Group F, Member 3 - drug effects ; periodontitis ; Periodontitis - immunology ; Periodontitis - microbiology ; Periodontitis - prevention & control ; Porphyromonas gingivalis - drug effects ; Porphyromonas gingivalis - immunology ; Random Allocation ; RANK ligand ; regulatory ; Spleen - pathology ; T-Lymphocytes, Regulatory - drug effects ; Th17 cells ; Th17 Cells - drug effects ; Transforming Growth Factor beta1 - drug effects ; tretinoin ; Tretinoin - administration & dosage ; Tretinoin - therapeutic use ; T‐lymphocytes</subject><ispartof>Journal of periodontology (1970), 2014-05, Vol.85 (5), p.740-750</ispartof><rights>2014 American Academy of Periodontology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4090-25914017df5c1e459af6bac9683cf5f75afa7fa1aded2d52571ba46d5865b3d13</citedby><cites>FETCH-LOGICAL-c4090-25914017df5c1e459af6bac9683cf5f75afa7fa1aded2d52571ba46d5865b3d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1902%2Fjop.2013.130132$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1902%2Fjop.2013.130132$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23952076$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Linyuan</creatorcontrib><creatorcontrib>Wang, Jinyan</creatorcontrib><creatorcontrib>Jin, Ying</creatorcontrib><creatorcontrib>Gao, Hong</creatorcontrib><creatorcontrib>Lin, Xiaoping</creatorcontrib><title>Oral Administration of All‐Trans Retinoic Acid Suppresses Experimental Periodontitis by Modulating the Th17/Treg Imbalance</title><title>Journal of periodontology (1970)</title><addtitle>J Periodontol</addtitle><description>Background: A T‐helper 17 (Th17)/regulatory T (Treg) imbalance has been suggested recently to play a role in the development of periodontitis. All‐trans retinoic acid (ATRA) has been reported to modulate Th17/Treg imbalances in some diseases. However, the effect of ATRA on periodontitis remains unknown. This study observes the effect of ATRA on Th17/Treg imbalance modulation in experimental periodontitis.
Methods: Experimental periodontitis was induced in mice by oral infection with Porphyromonas gingivalis (P. gingivalis). ATRA was orally administered every other day. Alveolar bone resorption (ABR) was estimated by measuring the distance from the cemento‐enamel junction to the alveolar bone crest. CD4+ T‐cell subsets in the cervical lymph nodes (CLNs) and spleen were analyzed by flow cytometry. Th17/Treg cell–related cytokine messenger ribonucleic acid expression was quantified by real‐time reverse transcription‐polymerase chain reaction.
Results: The present data shows that ATRA suppressed ABR and inhibited inflammatory cell infiltration into periodontal tissues. These effects were closely associated with reduced CD4+ retinoid‐related orphan receptor γτ+ cells and increased CD4+ forkhead box P3+ cells in the CLNs. Furthermore, ATRA downregulated interleukin (IL)‐17A expression and upregulated IL‐10 and transforming growth factor‐β1 expression in both the CLNs and P. gingivalis–infected gingival tissues.
Conclusions: These results suggest that ATRA modulation of the Th17/Treg imbalance provides protection against periodontitis by enhancing Treg cell activation and inhibiting Th17 cell activation. These results indicate the potential for clinical prevention of periodontitis.</description><subject>Administration, Oral</subject><subject>Alveolar Bone Loss - immunology</subject><subject>Alveolar Bone Loss - microbiology</subject><subject>Alveolar Bone Loss - prevention & control</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - administration & dosage</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Bone resorption</subject><subject>CD4-Positive T-Lymphocytes - drug effects</subject><subject>Dentistry</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Forkhead Transcription Factors - drug effects</subject><subject>Interleukin-10 - analysis</subject><subject>Interleukin-17 - analysis</subject><subject>Lymph Nodes - pathology</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred Strains</subject><subject>Nuclear Receptor Subfamily 1, Group F, Member 3 - drug effects</subject><subject>periodontitis</subject><subject>Periodontitis - immunology</subject><subject>Periodontitis - microbiology</subject><subject>Periodontitis - prevention & control</subject><subject>Porphyromonas gingivalis - drug effects</subject><subject>Porphyromonas gingivalis - immunology</subject><subject>Random Allocation</subject><subject>RANK ligand</subject><subject>regulatory</subject><subject>Spleen - pathology</subject><subject>T-Lymphocytes, Regulatory - drug effects</subject><subject>Th17 cells</subject><subject>Th17 Cells - drug effects</subject><subject>Transforming Growth Factor beta1 - drug effects</subject><subject>tretinoin</subject><subject>Tretinoin - administration & dosage</subject><subject>Tretinoin - therapeutic use</subject><subject>T‐lymphocytes</subject><issn>0022-3492</issn><issn>1943-3670</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1P3DAQhi3UCrYLZ26Vj71k1-OPhBxXaEupQCBYzpbjDzBK4tROVFbqgZ_Ab-wvqdFCr1w8HumdRzMPQsdAFlATunwMw4ISYAtg-aV7aAY1ZwUrK_IJzQihtGC8pgfoS0qPuQXOyD46oKwWlFTlDP25iqrFK9P53qcxqtGHHgeHV2379_llE1Wf8I0dfR-8xivtDb6dhiHalGzC66fBRt_ZfsyM6_wNJvSjH33CzRZfBjO1Gdjf4_HB4s0DVMtNtPf4vGtUq3ptD9Fnp9pkj97qHN19X29OfxQXV2fnp6uLQnNSk4KKGjiByjihwXJRK1c2StflCdNOuEoopyqnQBlrqBFUVNAoXhpxUoqGGWBz9G3HHWL4Ndk0ys4nbdu8hA1TkpBlABCegXO03EV1DClF6-SQL1RxK4HIV-UyK5evyuVOeZ74-gafms6a__l3xzkgdoHfvrXbj3jy5_X6hlScsH-YMY9H</recordid><startdate>201405</startdate><enddate>201405</enddate><creator>Wang, Linyuan</creator><creator>Wang, Jinyan</creator><creator>Jin, Ying</creator><creator>Gao, Hong</creator><creator>Lin, Xiaoping</creator><general>American Academy of Periodontology</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></search><sort><creationdate>201405</creationdate><title>Oral Administration of All‐Trans Retinoic Acid Suppresses Experimental Periodontitis by Modulating the Th17/Treg Imbalance</title><author>Wang, Linyuan ; Wang, Jinyan ; Jin, Ying ; Gao, Hong ; Lin, Xiaoping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4090-25914017df5c1e459af6bac9683cf5f75afa7fa1aded2d52571ba46d5865b3d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Administration, Oral</topic><topic>Alveolar Bone Loss - immunology</topic><topic>Alveolar Bone Loss - microbiology</topic><topic>Alveolar Bone Loss - prevention & control</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - administration & dosage</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Bone resorption</topic><topic>CD4-Positive T-Lymphocytes - drug effects</topic><topic>Dentistry</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Forkhead Transcription Factors - drug effects</topic><topic>Interleukin-10 - analysis</topic><topic>Interleukin-17 - analysis</topic><topic>Lymph Nodes - pathology</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred Strains</topic><topic>Nuclear Receptor Subfamily 1, Group F, Member 3 - drug effects</topic><topic>periodontitis</topic><topic>Periodontitis - immunology</topic><topic>Periodontitis - microbiology</topic><topic>Periodontitis - prevention & control</topic><topic>Porphyromonas gingivalis - drug effects</topic><topic>Porphyromonas gingivalis - immunology</topic><topic>Random Allocation</topic><topic>RANK ligand</topic><topic>regulatory</topic><topic>Spleen - pathology</topic><topic>T-Lymphocytes, Regulatory - drug effects</topic><topic>Th17 cells</topic><topic>Th17 Cells - drug effects</topic><topic>Transforming Growth Factor beta1 - drug effects</topic><topic>tretinoin</topic><topic>Tretinoin - administration & dosage</topic><topic>Tretinoin - therapeutic use</topic><topic>T‐lymphocytes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Linyuan</creatorcontrib><creatorcontrib>Wang, Jinyan</creatorcontrib><creatorcontrib>Jin, Ying</creatorcontrib><creatorcontrib>Gao, Hong</creatorcontrib><creatorcontrib>Lin, Xiaoping</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><jtitle>Journal of periodontology (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Linyuan</au><au>Wang, Jinyan</au><au>Jin, Ying</au><au>Gao, Hong</au><au>Lin, Xiaoping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oral Administration of All‐Trans Retinoic Acid Suppresses Experimental Periodontitis by Modulating the Th17/Treg Imbalance</atitle><jtitle>Journal of periodontology (1970)</jtitle><addtitle>J Periodontol</addtitle><date>2014-05</date><risdate>2014</risdate><volume>85</volume><issue>5</issue><spage>740</spage><epage>750</epage><pages>740-750</pages><issn>0022-3492</issn><eissn>1943-3670</eissn><abstract>Background: A T‐helper 17 (Th17)/regulatory T (Treg) imbalance has been suggested recently to play a role in the development of periodontitis. All‐trans retinoic acid (ATRA) has been reported to modulate Th17/Treg imbalances in some diseases. However, the effect of ATRA on periodontitis remains unknown. This study observes the effect of ATRA on Th17/Treg imbalance modulation in experimental periodontitis.
Methods: Experimental periodontitis was induced in mice by oral infection with Porphyromonas gingivalis (P. gingivalis). ATRA was orally administered every other day. Alveolar bone resorption (ABR) was estimated by measuring the distance from the cemento‐enamel junction to the alveolar bone crest. CD4+ T‐cell subsets in the cervical lymph nodes (CLNs) and spleen were analyzed by flow cytometry. Th17/Treg cell–related cytokine messenger ribonucleic acid expression was quantified by real‐time reverse transcription‐polymerase chain reaction.
Results: The present data shows that ATRA suppressed ABR and inhibited inflammatory cell infiltration into periodontal tissues. These effects were closely associated with reduced CD4+ retinoid‐related orphan receptor γτ+ cells and increased CD4+ forkhead box P3+ cells in the CLNs. Furthermore, ATRA downregulated interleukin (IL)‐17A expression and upregulated IL‐10 and transforming growth factor‐β1 expression in both the CLNs and P. gingivalis–infected gingival tissues.
Conclusions: These results suggest that ATRA modulation of the Th17/Treg imbalance provides protection against periodontitis by enhancing Treg cell activation and inhibiting Th17 cell activation. These results indicate the potential for clinical prevention of periodontitis.</abstract><cop>United States</cop><pub>American Academy of Periodontology</pub><pmid>23952076</pmid><doi>10.1902/jop.2013.130132</doi><tpages>11</tpages></addata></record> |
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| subjects | Administration, Oral Alveolar Bone Loss - immunology Alveolar Bone Loss - microbiology Alveolar Bone Loss - prevention & control Animals Anti-Inflammatory Agents - administration & dosage Anti-Inflammatory Agents - therapeutic use Bone resorption CD4-Positive T-Lymphocytes - drug effects Dentistry Disease Models, Animal Female Forkhead Transcription Factors - drug effects Interleukin-10 - analysis Interleukin-17 - analysis Lymph Nodes - pathology Lymphocyte Activation - drug effects Mice Mice, Inbred C57BL Mice, Inbred Strains Nuclear Receptor Subfamily 1, Group F, Member 3 - drug effects periodontitis Periodontitis - immunology Periodontitis - microbiology Periodontitis - prevention & control Porphyromonas gingivalis - drug effects Porphyromonas gingivalis - immunology Random Allocation RANK ligand regulatory Spleen - pathology T-Lymphocytes, Regulatory - drug effects Th17 cells Th17 Cells - drug effects Transforming Growth Factor beta1 - drug effects tretinoin Tretinoin - administration & dosage Tretinoin - therapeutic use T‐lymphocytes |
| title | Oral Administration of All‐Trans Retinoic Acid Suppresses Experimental Periodontitis by Modulating the Th17/Treg Imbalance |
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