IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA in patients with rheumatoid arthritis‐presenting periodontitis
Background Rheumatoid arthritis (RA) and periodontitis (P) are chronic inflammatory diseases characterized by joint and radiographic bone loss, respectively. IL‐23 and IL‐17 have an essential role in the immunopathogenesis of RA, and P. IL‐23 stimulates Th17 cells through which produces IL‐17, IL‐21...
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| Veröffentlicht in: | Journal of clinical laboratory analysis 2021-09, Vol.35 (9), p.e23963-n/a |
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| creator | Rodríguez‐Montaño, Ruth Bernard‐Medina, Ana Guilaisne Oregon‐Romero, Edith Martínez‐Rodríguez, Vianeth María del Carmen Pita‐López, María Luisa Gómez‐Meda, Belinda Claudia Guerrero‐Velázquez, Celia |
| description | Background
Rheumatoid arthritis (RA) and periodontitis (P) are chronic inflammatory diseases characterized by joint and radiographic bone loss, respectively. IL‐23 and IL‐17 have an essential role in the immunopathogenesis of RA, and P. IL‐23 stimulates Th17 cells through which produces IL‐17, IL‐21, and RANKL. IL‐17 stimulates fibroblasts to produce RANKL, which initiates bone loss in the joints in RA and the periodontal tissue in periodontitis. The aim of this study was to determine the expression pattern of IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA of patients with RA presenting P (RAP).
Material and methods
Healthy subjects (HS) (n = 42), patients with P (n = 40), RA (n = 20), and patients with RAP (n = 40) were included. Plasma samples were obtained to evaluate the IL‐23, IL‐17A, sIL‐23R, and sIL‐17RA by ELISA technique. A nonparametric Mann‐Whitney U test was used to compare the differences between groups. A Chi‐square was used to compare gender, grade and stage of periodontitis, and DAS28‐ESR between the groups. Spearman's rank correlation coefficient was used to study the association between the molecules and clinical parameters.
Results
IL‐23 levels were increased in the RAP group, and lower sIL‐23R levels were found in the RAP groups. However, IL‐17A was lower in the P and RAP group but not in RA patients. RAP group showed a decrease IL‐17A levels in advanced stages of the periodontal disease.
Conclusion
These results suggest that IL‐23 and IL‐17A tend to downregulate their expression patterns when patients present both rheumatoid arthritis and periodontitis.
Blood sample was taken to obtain plasma from all study participants. IL‐23, IL‐23R, IL‐17A, and IL‐17RA were detected with ELISA technique. Results: (a) The sIL‐23R levels were found lower in the RAP group and IL‐23 levels were increased. (b) IL‐17A was lower in the P and RAP group but not in RA patients. According to the chronicity of periodontitis, RAP group showed a decreased IL‐17A levels in advanced stages of the periodontal disease. |
| doi_str_mv | 10.1002/jcla.23963 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8418468</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2562521591</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4483-93e38a9d2fdc67326651dbafdaacf64114ee960a8dc4a8f24f9578e2cc0c5e2f3</originalsourceid><addsrcrecordid>eNp9kcuKFDEUhoMoTju68QEk4EaEmsmt0slGaBovIw3CoOuQTk5Np6mqlEmV4-x8AcFn9ElMT7WDunB1COc7H3_4EXpKyRklhJ3vXWvPGNeS30MLSrSqmGL1fbQgSi0rRSg_QY9y3hNClKbyITrhQhBeE71A3y82P7_9YPz8dtIltl9Dxrb3OMd22raAEzgYxpgyDjk2MXUZ5-PR5QweTy9XOPR4sGOAfsz4Oow7nHYwdXaMwWObxl0KY8gFHhLkAoX-Cg-QQvSxPMrqMXrQ2DbDk-M8RZ_evP64fldtPry9WK82lRNC8Upz4Mpqzxrv5JIzKWvqt7bx1rpGCkoFgJbEKu-EVQ0Tja6XCphzxNXAGn6KXs3eYdp24F3JkmxrhhQ6m25MtMH8venDzlzFL0YJqoRURfDiKEjx8wR5NF3IDtrW9hCnbFgtWc1orWlBn_-D7uOU-vK9A6WJokodhC9nyqWYc4LmLgwl5tCyObRsblsu8LM_49-hv2stAJ2B69DCzX9U5v16s5qlvwD9Crkd</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2569081888</pqid></control><display><type>article</type><title>IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA in patients with rheumatoid arthritis‐presenting periodontitis</title><source>MEDLINE</source><source>Wiley Journals</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Rodríguez‐Montaño, Ruth ; Bernard‐Medina, Ana Guilaisne ; Oregon‐Romero, Edith ; Martínez‐Rodríguez, Vianeth María del Carmen ; Pita‐López, María Luisa ; Gómez‐Meda, Belinda Claudia ; Guerrero‐Velázquez, Celia</creator><creatorcontrib>Rodríguez‐Montaño, Ruth ; Bernard‐Medina, Ana Guilaisne ; Oregon‐Romero, Edith ; Martínez‐Rodríguez, Vianeth María del Carmen ; Pita‐López, María Luisa ; Gómez‐Meda, Belinda Claudia ; Guerrero‐Velázquez, Celia</creatorcontrib><description>Background
Rheumatoid arthritis (RA) and periodontitis (P) are chronic inflammatory diseases characterized by joint and radiographic bone loss, respectively. IL‐23 and IL‐17 have an essential role in the immunopathogenesis of RA, and P. IL‐23 stimulates Th17 cells through which produces IL‐17, IL‐21, and RANKL. IL‐17 stimulates fibroblasts to produce RANKL, which initiates bone loss in the joints in RA and the periodontal tissue in periodontitis. The aim of this study was to determine the expression pattern of IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA of patients with RA presenting P (RAP).
Material and methods
Healthy subjects (HS) (n = 42), patients with P (n = 40), RA (n = 20), and patients with RAP (n = 40) were included. Plasma samples were obtained to evaluate the IL‐23, IL‐17A, sIL‐23R, and sIL‐17RA by ELISA technique. A nonparametric Mann‐Whitney U test was used to compare the differences between groups. A Chi‐square was used to compare gender, grade and stage of periodontitis, and DAS28‐ESR between the groups. Spearman's rank correlation coefficient was used to study the association between the molecules and clinical parameters.
Results
IL‐23 levels were increased in the RAP group, and lower sIL‐23R levels were found in the RAP groups. However, IL‐17A was lower in the P and RAP group but not in RA patients. RAP group showed a decrease IL‐17A levels in advanced stages of the periodontal disease.
Conclusion
These results suggest that IL‐23 and IL‐17A tend to downregulate their expression patterns when patients present both rheumatoid arthritis and periodontitis.
Blood sample was taken to obtain plasma from all study participants. IL‐23, IL‐23R, IL‐17A, and IL‐17RA were detected with ELISA technique. Results: (a) The sIL‐23R levels were found lower in the RAP group and IL‐23 levels were increased. (b) IL‐17A was lower in the P and RAP group but not in RA patients. According to the chronicity of periodontitis, RAP group showed a decreased IL‐17A levels in advanced stages of the periodontal disease.</description><identifier>ISSN: 0887-8013</identifier><identifier>EISSN: 1098-2825</identifier><identifier>DOI: 10.1002/jcla.23963</identifier><identifier>PMID: 34403509</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Adult ; Arthritis, Rheumatoid - blood ; Arthritis, Rheumatoid - complications ; Arthritis, Rheumatoid - pathology ; Biomarkers ; Bone loss ; Case-Control Studies ; Cross-Sectional Studies ; Disease ; Enzyme-linked immunosorbent assay ; Female ; Fibroblasts ; Gum disease ; Helper cells ; Hospitals ; Humans ; IL‐17A ; IL‐23 ; Immunopathogenesis ; Inflammation ; Inflammatory diseases ; Interleukin-17 - blood ; Interleukin-23 Subunit p19 - blood ; Isoforms ; Joint diseases ; Lymphocytes T ; Male ; Patients ; Periodontal diseases ; Periodontics ; Periodontitis ; Periodontitis - blood ; Periodontitis - complications ; Periodontitis - pathology ; Plasma ; Prognosis ; Receptors, Interleukin - blood ; Receptors, Interleukin-17 - blood ; Rheumatoid arthritis ; rheumatoid arthritis‐presenting periodontitis ; Rheumatology ; sIL‐17RA ; sIL‐23R ; Software ; TRANCE protein</subject><ispartof>Journal of clinical laboratory analysis, 2021-09, Vol.35 (9), p.e23963-n/a</ispartof><rights>2021 The Authors. published by Wiley Periodicals LLC</rights><rights>2021 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4483-93e38a9d2fdc67326651dbafdaacf64114ee960a8dc4a8f24f9578e2cc0c5e2f3</citedby><cites>FETCH-LOGICAL-c4483-93e38a9d2fdc67326651dbafdaacf64114ee960a8dc4a8f24f9578e2cc0c5e2f3</cites><orcidid>0000-0001-6010-0837 ; 0000-0003-0775-8810</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8418468/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8418468/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34403509$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rodríguez‐Montaño, Ruth</creatorcontrib><creatorcontrib>Bernard‐Medina, Ana Guilaisne</creatorcontrib><creatorcontrib>Oregon‐Romero, Edith</creatorcontrib><creatorcontrib>Martínez‐Rodríguez, Vianeth María del Carmen</creatorcontrib><creatorcontrib>Pita‐López, María Luisa</creatorcontrib><creatorcontrib>Gómez‐Meda, Belinda Claudia</creatorcontrib><creatorcontrib>Guerrero‐Velázquez, Celia</creatorcontrib><title>IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA in patients with rheumatoid arthritis‐presenting periodontitis</title><title>Journal of clinical laboratory analysis</title><addtitle>J Clin Lab Anal</addtitle><description>Background
Rheumatoid arthritis (RA) and periodontitis (P) are chronic inflammatory diseases characterized by joint and radiographic bone loss, respectively. IL‐23 and IL‐17 have an essential role in the immunopathogenesis of RA, and P. IL‐23 stimulates Th17 cells through which produces IL‐17, IL‐21, and RANKL. IL‐17 stimulates fibroblasts to produce RANKL, which initiates bone loss in the joints in RA and the periodontal tissue in periodontitis. The aim of this study was to determine the expression pattern of IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA of patients with RA presenting P (RAP).
Material and methods
Healthy subjects (HS) (n = 42), patients with P (n = 40), RA (n = 20), and patients with RAP (n = 40) were included. Plasma samples were obtained to evaluate the IL‐23, IL‐17A, sIL‐23R, and sIL‐17RA by ELISA technique. A nonparametric Mann‐Whitney U test was used to compare the differences between groups. A Chi‐square was used to compare gender, grade and stage of periodontitis, and DAS28‐ESR between the groups. Spearman's rank correlation coefficient was used to study the association between the molecules and clinical parameters.
Results
IL‐23 levels were increased in the RAP group, and lower sIL‐23R levels were found in the RAP groups. However, IL‐17A was lower in the P and RAP group but not in RA patients. RAP group showed a decrease IL‐17A levels in advanced stages of the periodontal disease.
Conclusion
These results suggest that IL‐23 and IL‐17A tend to downregulate their expression patterns when patients present both rheumatoid arthritis and periodontitis.
Blood sample was taken to obtain plasma from all study participants. IL‐23, IL‐23R, IL‐17A, and IL‐17RA were detected with ELISA technique. Results: (a) The sIL‐23R levels were found lower in the RAP group and IL‐23 levels were increased. (b) IL‐17A was lower in the P and RAP group but not in RA patients. According to the chronicity of periodontitis, RAP group showed a decreased IL‐17A levels in advanced stages of the periodontal disease.</description><subject>Adult</subject><subject>Arthritis, Rheumatoid - blood</subject><subject>Arthritis, Rheumatoid - complications</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Biomarkers</subject><subject>Bone loss</subject><subject>Case-Control Studies</subject><subject>Cross-Sectional Studies</subject><subject>Disease</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Gum disease</subject><subject>Helper cells</subject><subject>Hospitals</subject><subject>Humans</subject><subject>IL‐17A</subject><subject>IL‐23</subject><subject>Immunopathogenesis</subject><subject>Inflammation</subject><subject>Inflammatory diseases</subject><subject>Interleukin-17 - blood</subject><subject>Interleukin-23 Subunit p19 - blood</subject><subject>Isoforms</subject><subject>Joint diseases</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Patients</subject><subject>Periodontal diseases</subject><subject>Periodontics</subject><subject>Periodontitis</subject><subject>Periodontitis - blood</subject><subject>Periodontitis - complications</subject><subject>Periodontitis - pathology</subject><subject>Plasma</subject><subject>Prognosis</subject><subject>Receptors, Interleukin - blood</subject><subject>Receptors, Interleukin-17 - blood</subject><subject>Rheumatoid arthritis</subject><subject>rheumatoid arthritis‐presenting periodontitis</subject><subject>Rheumatology</subject><subject>sIL‐17RA</subject><subject>sIL‐23R</subject><subject>Software</subject><subject>TRANCE protein</subject><issn>0887-8013</issn><issn>1098-2825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kcuKFDEUhoMoTju68QEk4EaEmsmt0slGaBovIw3CoOuQTk5Np6mqlEmV4-x8AcFn9ElMT7WDunB1COc7H3_4EXpKyRklhJ3vXWvPGNeS30MLSrSqmGL1fbQgSi0rRSg_QY9y3hNClKbyITrhQhBeE71A3y82P7_9YPz8dtIltl9Dxrb3OMd22raAEzgYxpgyDjk2MXUZ5-PR5QweTy9XOPR4sGOAfsz4Oow7nHYwdXaMwWObxl0KY8gFHhLkAoX-Cg-QQvSxPMrqMXrQ2DbDk-M8RZ_evP64fldtPry9WK82lRNC8Upz4Mpqzxrv5JIzKWvqt7bx1rpGCkoFgJbEKu-EVQ0Tja6XCphzxNXAGn6KXs3eYdp24F3JkmxrhhQ6m25MtMH8venDzlzFL0YJqoRURfDiKEjx8wR5NF3IDtrW9hCnbFgtWc1orWlBn_-D7uOU-vK9A6WJokodhC9nyqWYc4LmLgwl5tCyObRsblsu8LM_49-hv2stAJ2B69DCzX9U5v16s5qlvwD9Crkd</recordid><startdate>202109</startdate><enddate>202109</enddate><creator>Rodríguez‐Montaño, Ruth</creator><creator>Bernard‐Medina, Ana Guilaisne</creator><creator>Oregon‐Romero, Edith</creator><creator>Martínez‐Rodríguez, Vianeth María del Carmen</creator><creator>Pita‐López, María Luisa</creator><creator>Gómez‐Meda, Belinda Claudia</creator><creator>Guerrero‐Velázquez, Celia</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7T5</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>8C1</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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6010-0837</orcidid><orcidid>https://orcid.org/0000-0003-0775-8810</orcidid></search><sort><creationdate>202109</creationdate><title>IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA in patients with rheumatoid arthritis‐presenting periodontitis</title><author>Rodríguez‐Montaño, Ruth ; Bernard‐Medina, Ana Guilaisne ; Oregon‐Romero, Edith ; Martínez‐Rodríguez, Vianeth María del Carmen ; Pita‐López, María Luisa ; Gómez‐Meda, Belinda Claudia ; Guerrero‐Velázquez, Celia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4483-93e38a9d2fdc67326651dbafdaacf64114ee960a8dc4a8f24f9578e2cc0c5e2f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adult</topic><topic>Arthritis, Rheumatoid - blood</topic><topic>Arthritis, Rheumatoid - complications</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Biomarkers</topic><topic>Bone loss</topic><topic>Case-Control Studies</topic><topic>Cross-Sectional Studies</topic><topic>Disease</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Gum disease</topic><topic>Helper cells</topic><topic>Hospitals</topic><topic>Humans</topic><topic>IL‐17A</topic><topic>IL‐23</topic><topic>Immunopathogenesis</topic><topic>Inflammation</topic><topic>Inflammatory diseases</topic><topic>Interleukin-17 - blood</topic><topic>Interleukin-23 Subunit p19 - blood</topic><topic>Isoforms</topic><topic>Joint diseases</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Patients</topic><topic>Periodontal diseases</topic><topic>Periodontics</topic><topic>Periodontitis</topic><topic>Periodontitis - blood</topic><topic>Periodontitis - complications</topic><topic>Periodontitis - pathology</topic><topic>Plasma</topic><topic>Prognosis</topic><topic>Receptors, Interleukin - blood</topic><topic>Receptors, Interleukin-17 - blood</topic><topic>Rheumatoid arthritis</topic><topic>rheumatoid arthritis‐presenting periodontitis</topic><topic>Rheumatology</topic><topic>sIL‐17RA</topic><topic>sIL‐23R</topic><topic>Software</topic><topic>TRANCE protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rodríguez‐Montaño, Ruth</creatorcontrib><creatorcontrib>Bernard‐Medina, Ana Guilaisne</creatorcontrib><creatorcontrib>Oregon‐Romero, Edith</creatorcontrib><creatorcontrib>Martínez‐Rodríguez, Vianeth María del Carmen</creatorcontrib><creatorcontrib>Pita‐López, María Luisa</creatorcontrib><creatorcontrib>Gómez‐Meda, Belinda Claudia</creatorcontrib><creatorcontrib>Guerrero‐Velázquez, Celia</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Public Health Database</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical laboratory analysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rodríguez‐Montaño, Ruth</au><au>Bernard‐Medina, Ana Guilaisne</au><au>Oregon‐Romero, Edith</au><au>Martínez‐Rodríguez, Vianeth María del Carmen</au><au>Pita‐López, María Luisa</au><au>Gómez‐Meda, Belinda Claudia</au><au>Guerrero‐Velázquez, Celia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA in patients with rheumatoid arthritis‐presenting periodontitis</atitle><jtitle>Journal of clinical laboratory analysis</jtitle><addtitle>J Clin Lab Anal</addtitle><date>2021-09</date><risdate>2021</risdate><volume>35</volume><issue>9</issue><spage>e23963</spage><epage>n/a</epage><pages>e23963-n/a</pages><issn>0887-8013</issn><eissn>1098-2825</eissn><abstract>Background
Rheumatoid arthritis (RA) and periodontitis (P) are chronic inflammatory diseases characterized by joint and radiographic bone loss, respectively. IL‐23 and IL‐17 have an essential role in the immunopathogenesis of RA, and P. IL‐23 stimulates Th17 cells through which produces IL‐17, IL‐21, and RANKL. IL‐17 stimulates fibroblasts to produce RANKL, which initiates bone loss in the joints in RA and the periodontal tissue in periodontitis. The aim of this study was to determine the expression pattern of IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA of patients with RA presenting P (RAP).
Material and methods
Healthy subjects (HS) (n = 42), patients with P (n = 40), RA (n = 20), and patients with RAP (n = 40) were included. Plasma samples were obtained to evaluate the IL‐23, IL‐17A, sIL‐23R, and sIL‐17RA by ELISA technique. A nonparametric Mann‐Whitney U test was used to compare the differences between groups. A Chi‐square was used to compare gender, grade and stage of periodontitis, and DAS28‐ESR between the groups. Spearman's rank correlation coefficient was used to study the association between the molecules and clinical parameters.
Results
IL‐23 levels were increased in the RAP group, and lower sIL‐23R levels were found in the RAP groups. However, IL‐17A was lower in the P and RAP group but not in RA patients. RAP group showed a decrease IL‐17A levels in advanced stages of the periodontal disease.
Conclusion
These results suggest that IL‐23 and IL‐17A tend to downregulate their expression patterns when patients present both rheumatoid arthritis and periodontitis.
Blood sample was taken to obtain plasma from all study participants. IL‐23, IL‐23R, IL‐17A, and IL‐17RA were detected with ELISA technique. Results: (a) The sIL‐23R levels were found lower in the RAP group and IL‐23 levels were increased. (b) IL‐17A was lower in the P and RAP group but not in RA patients. According to the chronicity of periodontitis, RAP group showed a decreased IL‐17A levels in advanced stages of the periodontal disease.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>34403509</pmid><doi>10.1002/jcla.23963</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-6010-0837</orcidid><orcidid>https://orcid.org/0000-0003-0775-8810</orcidid><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8418468 |
| source | MEDLINE; Wiley Journals; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Adult Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - complications Arthritis, Rheumatoid - pathology Biomarkers Bone loss Case-Control Studies Cross-Sectional Studies Disease Enzyme-linked immunosorbent assay Female Fibroblasts Gum disease Helper cells Hospitals Humans IL‐17A IL‐23 Immunopathogenesis Inflammation Inflammatory diseases Interleukin-17 - blood Interleukin-23 Subunit p19 - blood Isoforms Joint diseases Lymphocytes T Male Patients Periodontal diseases Periodontics Periodontitis Periodontitis - blood Periodontitis - complications Periodontitis - pathology Plasma Prognosis Receptors, Interleukin - blood Receptors, Interleukin-17 - blood Rheumatoid arthritis rheumatoid arthritis‐presenting periodontitis Rheumatology sIL‐17RA sIL‐23R Software TRANCE protein |
| title | IL‐23/IL‐17 axis and soluble receptors isoforms sIL‐23R and sIL‐17RA in patients with rheumatoid arthritis‐presenting periodontitis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T00%3A32%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=IL%E2%80%9023/IL%E2%80%9017%20axis%20and%20soluble%20receptors%20isoforms%20sIL%E2%80%9023R%20and%20sIL%E2%80%9017RA%20in%20patients%20with%20rheumatoid%20arthritis%E2%80%90presenting%20periodontitis&rft.jtitle=Journal%20of%20clinical%20laboratory%20analysis&rft.au=Rodr%C3%ADguez%E2%80%90Monta%C3%B1o,%20Ruth&rft.date=2021-09&rft.volume=35&rft.issue=9&rft.spage=e23963&rft.epage=n/a&rft.pages=e23963-n/a&rft.issn=0887-8013&rft.eissn=1098-2825&rft_id=info:doi/10.1002/jcla.23963&rft_dat=%3Cproquest_pubme%3E2562521591%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2569081888&rft_id=info:pmid/34403509&rfr_iscdi=true |