Reduction of Oxidative Stress in Peripheral Blood Mononuclear Cells Attenuates the Inflammatory Response of Fibroblast-like Synoviocytes in Rheumatoid Arthritis
The production and oxidation mechanism of reactive oxygen species (ROS) are out of balance in rheumatoid arthritis (RA). However, the correlation between ROS and T cell subsets in RA remains unclear. Peripheral blood mononuclear cells (PBMCs) from patients with RA (n = 40) and healthy controls (n =...
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| Veröffentlicht in: | International journal of molecular sciences 2021-11, Vol.22 (22), p.12411 |
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| description | The production and oxidation mechanism of reactive oxygen species (ROS) are out of balance in rheumatoid arthritis (RA). However, the correlation between ROS and T cell subsets in RA remains unclear. Peripheral blood mononuclear cells (PBMCs) from patients with RA (n = 40) and healthy controls (n = 10) were isolated from whole blood samples. Synovial tissues (n = 3) and synovial fluid (n = 10) were obtained from patients with RA. The repartition of T cell subsets and expression of ROS and cytokines were examined according to RA severity. Fibroblast-like synoviocytes (FLSs) from patients with RA were stimulated with PBMCs and the expression of inflammation-related molecules were measured by RT-PCR and cytokine array. Regulatory T cells from patients with moderate (5.1 > DAS28 ≥ 3.2) RA showed the highest expression of mitochondrial ROS among the groups based on disease severity. Although ROS levels steadily increased with RA severity, there was a slight decline in severe RA (DAS28 ≥ 5.1) compared with moderate RA. The expression of inflammatory cytokines in RA FLSs were significantly inhibited when FLSs were co-cultured with PBMCs treated with ROS inhibitor. These findings provide a novel approach to suppress inflammatory response of FLSs through ROS regulation in PBMCs. |
| doi_str_mv | 10.3390/ijms222212411 |
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However, the correlation between ROS and T cell subsets in RA remains unclear. Peripheral blood mononuclear cells (PBMCs) from patients with RA (n = 40) and healthy controls (n = 10) were isolated from whole blood samples. Synovial tissues (n = 3) and synovial fluid (n = 10) were obtained from patients with RA. The repartition of T cell subsets and expression of ROS and cytokines were examined according to RA severity. Fibroblast-like synoviocytes (FLSs) from patients with RA were stimulated with PBMCs and the expression of inflammation-related molecules were measured by RT-PCR and cytokine array. Regulatory T cells from patients with moderate (5.1 > DAS28 ≥ 3.2) RA showed the highest expression of mitochondrial ROS among the groups based on disease severity. Although ROS levels steadily increased with RA severity, there was a slight decline in severe RA (DAS28 ≥ 5.1) compared with moderate RA. The expression of inflammatory cytokines in RA FLSs were significantly inhibited when FLSs were co-cultured with PBMCs treated with ROS inhibitor. These findings provide a novel approach to suppress inflammatory response of FLSs through ROS regulation in PBMCs.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms222212411</identifier><identifier>PMID: 34830290</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Arthritis ; Arthritis, Rheumatoid - blood ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - pathology ; Blood ; Case-Control Studies ; Cells, Cultured ; Chemokines ; Coculture Techniques ; Cytokines ; Cytokines - metabolism ; Disease ; Female ; Fibroblasts ; Fibroblasts - immunology ; Gene expression ; Homeostasis ; Humans ; Hyperplasia ; Immunoregulation ; Inflammation ; Inflammation - metabolism ; Inflammatory response ; Leukocytes (mononuclear) ; Lymphocytes ; Lymphocytes T ; Male ; Middle Aged ; Mitochondria ; Mitochondria - metabolism ; Oxidation ; Oxidative Stress ; Pathogenesis ; Peripheral blood mononuclear cells ; Polymerase chain reaction ; Population ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Rheumatoid arthritis ; Severity of Illness Index ; Synovial fluid ; Synovial Fluid - metabolism ; Synoviocytes ; Synoviocytes - immunology ; T cell receptors ; T-Lymphocytes, Helper-Inducer - immunology ; T-Lymphocytes, Regulatory - immunology ; Tumor necrosis factor-TNF</subject><ispartof>International journal of molecular sciences, 2021-11, Vol.22 (22), p.12411</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-da3a4556e737a55c52bba05d6b3d40448982489170ab41228f8f074e090e00b33</citedby><cites>FETCH-LOGICAL-c415t-da3a4556e737a55c52bba05d6b3d40448982489170ab41228f8f074e090e00b33</cites><orcidid>0000-0003-4620-8803 ; 0000-0002-0076-0822</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/PMC8624216/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8624216/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34830290$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Ha-Reum</creatorcontrib><creatorcontrib>Yoo, Su-Jin</creatorcontrib><creatorcontrib>Kim, Jinhyun</creatorcontrib><creatorcontrib>Park, Chan Keol</creatorcontrib><creatorcontrib>Kang, Seong Wook</creatorcontrib><title>Reduction of Oxidative Stress in Peripheral Blood Mononuclear Cells Attenuates the Inflammatory Response of Fibroblast-like Synoviocytes in Rheumatoid Arthritis</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>The production and oxidation mechanism of reactive oxygen species (ROS) are out of balance in rheumatoid arthritis (RA). However, the correlation between ROS and T cell subsets in RA remains unclear. Peripheral blood mononuclear cells (PBMCs) from patients with RA (n = 40) and healthy controls (n = 10) were isolated from whole blood samples. Synovial tissues (n = 3) and synovial fluid (n = 10) were obtained from patients with RA. The repartition of T cell subsets and expression of ROS and cytokines were examined according to RA severity. Fibroblast-like synoviocytes (FLSs) from patients with RA were stimulated with PBMCs and the expression of inflammation-related molecules were measured by RT-PCR and cytokine array. Regulatory T cells from patients with moderate (5.1 > DAS28 ≥ 3.2) RA showed the highest expression of mitochondrial ROS among the groups based on disease severity. Although ROS levels steadily increased with RA severity, there was a slight decline in severe RA (DAS28 ≥ 5.1) compared with moderate RA. The expression of inflammatory cytokines in RA FLSs were significantly inhibited when FLSs were co-cultured with PBMCs treated with ROS inhibitor. These findings provide a novel approach to suppress inflammatory response of FLSs through ROS regulation in PBMCs.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Arthritis</subject><subject>Arthritis, Rheumatoid - blood</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Blood</subject><subject>Case-Control Studies</subject><subject>Cells, Cultured</subject><subject>Chemokines</subject><subject>Coculture Techniques</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Disease</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Fibroblasts - immunology</subject><subject>Gene expression</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Immunoregulation</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory response</subject><subject>Leukocytes (mononuclear)</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Oxidation</subject><subject>Oxidative Stress</subject><subject>Pathogenesis</subject><subject>Peripheral blood mononuclear cells</subject><subject>Polymerase chain reaction</subject><subject>Population</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rheumatoid arthritis</subject><subject>Severity of Illness Index</subject><subject>Synovial fluid</subject><subject>Synovial Fluid - metabolism</subject><subject>Synoviocytes</subject><subject>Synoviocytes - immunology</subject><subject>T cell receptors</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Tumor necrosis factor-TNF</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUtv1DAUhS0EoqWwZIsssWETev3KY4M0jFqoVFQ0wDpykhviIbGntjPq_Bt-Ko76UIsXtiV_99x7fAh5y-CjEBWcmu0UeFqMS8aekWMmOc8A8uL5o_sReRXCFoALrqqX5EjIUgCv4Jj83WA3t9E4S11Pr25Mp6PZI_0RPYZAjaXf0ZvdgF6P9PPoXEe_Oevs3I6oPV3jOAa6ihHtrCMGGgekF7Yf9TTp6PyBbjDsnA24yJ-bxrtm1CFmo_mTmhys2xvXHpbK1Goz4LyUmY6ufBy8iSa8Ji96PQZ8c3eekF_nZz_XX7PLqy8X69Vl1kqmYtZpoaVSORai0Eq1ijeNBtXljegkSFlWJU8bK0A3knFe9mUPhUSoAAEaIU7Ip1vd3dxM2LVoY7Jc77yZtD_UTpv66Ys1Q_3b7esy55KzPAl8uBPw7nrGEOvJhDb9j7bo5lDzHCSwNEaZ0Pf_oVs3e5vsLRRnTAmQicpuqda7EDz2D8MwqJfs6yfZJ_7dYwcP9H3Y4h9b5q3P</recordid><startdate>20211117</startdate><enddate>20211117</enddate><creator>Lee, Ha-Reum</creator><creator>Yoo, Su-Jin</creator><creator>Kim, Jinhyun</creator><creator>Park, Chan Keol</creator><creator>Kang, Seong Wook</creator><general>MDPI AG</general><general>MDPI</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4620-8803</orcidid><orcidid>https://orcid.org/0000-0002-0076-0822</orcidid></search><sort><creationdate>20211117</creationdate><title>Reduction of Oxidative Stress in Peripheral Blood Mononuclear Cells Attenuates the Inflammatory Response of Fibroblast-like Synoviocytes in Rheumatoid Arthritis</title><author>Lee, Ha-Reum ; Yoo, Su-Jin ; Kim, Jinhyun ; Park, Chan Keol ; Kang, Seong Wook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-da3a4556e737a55c52bba05d6b3d40448982489170ab41228f8f074e090e00b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Arthritis</topic><topic>Arthritis, Rheumatoid - blood</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Blood</topic><topic>Case-Control Studies</topic><topic>Cells, Cultured</topic><topic>Chemokines</topic><topic>Coculture Techniques</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Disease</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Fibroblasts - immunology</topic><topic>Gene expression</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Immunoregulation</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory response</topic><topic>Leukocytes (mononuclear)</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Oxidation</topic><topic>Oxidative Stress</topic><topic>Pathogenesis</topic><topic>Peripheral blood mononuclear cells</topic><topic>Polymerase chain reaction</topic><topic>Population</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rheumatoid arthritis</topic><topic>Severity of Illness Index</topic><topic>Synovial fluid</topic><topic>Synovial Fluid - metabolism</topic><topic>Synoviocytes</topic><topic>Synoviocytes - immunology</topic><topic>T cell receptors</topic><topic>T-Lymphocytes, Helper-Inducer - immunology</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Ha-Reum</creatorcontrib><creatorcontrib>Yoo, Su-Jin</creatorcontrib><creatorcontrib>Kim, Jinhyun</creatorcontrib><creatorcontrib>Park, Chan Keol</creatorcontrib><creatorcontrib>Kang, Seong Wook</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Ha-Reum</au><au>Yoo, Su-Jin</au><au>Kim, Jinhyun</au><au>Park, Chan Keol</au><au>Kang, Seong Wook</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction of Oxidative Stress in Peripheral Blood Mononuclear Cells Attenuates the Inflammatory Response of Fibroblast-like Synoviocytes in Rheumatoid Arthritis</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2021-11-17</date><risdate>2021</risdate><volume>22</volume><issue>22</issue><spage>12411</spage><pages>12411-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The production and oxidation mechanism of reactive oxygen species (ROS) are out of balance in rheumatoid arthritis (RA). However, the correlation between ROS and T cell subsets in RA remains unclear. Peripheral blood mononuclear cells (PBMCs) from patients with RA (n = 40) and healthy controls (n = 10) were isolated from whole blood samples. Synovial tissues (n = 3) and synovial fluid (n = 10) were obtained from patients with RA. The repartition of T cell subsets and expression of ROS and cytokines were examined according to RA severity. Fibroblast-like synoviocytes (FLSs) from patients with RA were stimulated with PBMCs and the expression of inflammation-related molecules were measured by RT-PCR and cytokine array. Regulatory T cells from patients with moderate (5.1 > DAS28 ≥ 3.2) RA showed the highest expression of mitochondrial ROS among the groups based on disease severity. Although ROS levels steadily increased with RA severity, there was a slight decline in severe RA (DAS28 ≥ 5.1) compared with moderate RA. The expression of inflammatory cytokines in RA FLSs were significantly inhibited when FLSs were co-cultured with PBMCs treated with ROS inhibitor. These findings provide a novel approach to suppress inflammatory response of FLSs through ROS regulation in PBMCs.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>34830290</pmid><doi>10.3390/ijms222212411</doi><orcidid>https://orcid.org/0000-0003-4620-8803</orcidid><orcidid>https://orcid.org/0000-0002-0076-0822</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Aged, 80 and over Arthritis Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - pathology Blood Case-Control Studies Cells, Cultured Chemokines Coculture Techniques Cytokines Cytokines - metabolism Disease Female Fibroblasts Fibroblasts - immunology Gene expression Homeostasis Humans Hyperplasia Immunoregulation Inflammation Inflammation - metabolism Inflammatory response Leukocytes (mononuclear) Lymphocytes Lymphocytes T Male Middle Aged Mitochondria Mitochondria - metabolism Oxidation Oxidative Stress Pathogenesis Peripheral blood mononuclear cells Polymerase chain reaction Population Reactive oxygen species Reactive Oxygen Species - metabolism Rheumatoid arthritis Severity of Illness Index Synovial fluid Synovial Fluid - metabolism Synoviocytes Synoviocytes - immunology T cell receptors T-Lymphocytes, Helper-Inducer - immunology T-Lymphocytes, Regulatory - immunology Tumor necrosis factor-TNF |
| title | Reduction of Oxidative Stress in Peripheral Blood Mononuclear Cells Attenuates the Inflammatory Response of Fibroblast-like Synoviocytes in Rheumatoid Arthritis |
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