Immunohistochemical study of interleukin-1β and interleukin-1 receptor antagonist in an antigen-induced arthritis of the rabbit temporomandibular joint
Background: In temporomandibular joint (TMJ) arthritis, there is limited knowledge of the relationship between interleukin‐1β (IL‐1β) and interleukin‐1 receptor antagonist (IL‐1ra), as well as the source of these cytokines. We investigated the development of an antigen‐induced arthritis in the rabb...
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| Veröffentlicht in: | Journal of oral pathology & medicine 2002-01, Vol.31 (1), p.45-54 |
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| creator | Habu, Manabu Tominaga, Kazuhiro Sukedai, Miho Alstergren, Per Ohkawara, Susumu Kopp, Sigvard Fukuda, Jinichi |
| description | Background: In temporomandibular joint (TMJ) arthritis, there is limited knowledge of the relationship between interleukin‐1β (IL‐1β) and interleukin‐1 receptor antagonist (IL‐1ra), as well as the source of these cytokines. We investigated the development of an antigen‐induced arthritis in the rabbit TMJ immunohistochemically.
Methods: Unilateral TMJ arthritis was induced in 32 adult New Zealand White rabbits. From 6 h to 12 weeks after induction of arthritis, topology of IL‐1β and IL‐1ra were observed.
Result: The acute stage of induced arthritis lasted for one week after induction, thereafter it became chronic. In the early phase of the acute stage, infiltrating inflammatory cells, as well as synovial cells, produced IL‐1β and IL‐1ra. In the late phase of the acute stage, the main source of these cytokines was subsynovial fibroblasts. In this phase of arthritis, IL‐1β and IL‐1ra did not appear to be produced by synovial cells. From the early to intermediate phase of the chronic stage, proliferating synovial cells produced IL‐1β and IL‐1ra. In this phase of the arthritis, these cytokines were also observed in a cluster formation in chondrocytes.
Conclusion: This arthritis model shows a staging of the joint inflammation process with time. IL‐1β and IL‐1ra are produced by a certain kind of cells depending on the stage of inflammation. |
| doi_str_mv | 10.1046/j.0904-2512.2001.10057.x |
| format | Article |
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Methods: Unilateral TMJ arthritis was induced in 32 adult New Zealand White rabbits. From 6 h to 12 weeks after induction of arthritis, topology of IL‐1β and IL‐1ra were observed.
Result: The acute stage of induced arthritis lasted for one week after induction, thereafter it became chronic. In the early phase of the acute stage, infiltrating inflammatory cells, as well as synovial cells, produced IL‐1β and IL‐1ra. In the late phase of the acute stage, the main source of these cytokines was subsynovial fibroblasts. In this phase of arthritis, IL‐1β and IL‐1ra did not appear to be produced by synovial cells. From the early to intermediate phase of the chronic stage, proliferating synovial cells produced IL‐1β and IL‐1ra. In this phase of the arthritis, these cytokines were also observed in a cluster formation in chondrocytes.
Conclusion: This arthritis model shows a staging of the joint inflammation process with time. IL‐1β and IL‐1ra are produced by a certain kind of cells depending on the stage of inflammation.</description><identifier>ISSN: 0904-2512</identifier><identifier>EISSN: 1600-0714</identifier><identifier>DOI: 10.1046/j.0904-2512.2001.10057.x</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science, Ltd</publisher><subject>antigen-induced arthritis ; Biological and medical sciences ; Diseases of the osteoarticular system ; Facial bones, jaws, teeth, parodontium: diseases, semeiology ; immunohistochemistry ; Inflammatory joint diseases ; interleukin-1 receptor antagonist ; interleukin-1β ; Medical sciences ; Non tumoral diseases ; Otorhinolaryngology. Stomatology ; rabbit ; temporomandibular joint</subject><ispartof>Journal of oral pathology & medicine, 2002-01, Vol.31 (1), p.45-54</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5008-37ed964dffdfe84e47b1f39a22b7cbdc7c264e69c3faddb5f44c6e715340eca63</citedby><cites>FETCH-LOGICAL-c5008-37ed964dffdfe84e47b1f39a22b7cbdc7c264e69c3faddb5f44c6e715340eca63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.0904-2512.2001.10057.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.0904-2512.2001.10057.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,4024,27923,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13586574$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1936370$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Habu, Manabu</creatorcontrib><creatorcontrib>Tominaga, Kazuhiro</creatorcontrib><creatorcontrib>Sukedai, Miho</creatorcontrib><creatorcontrib>Alstergren, Per</creatorcontrib><creatorcontrib>Ohkawara, Susumu</creatorcontrib><creatorcontrib>Kopp, Sigvard</creatorcontrib><creatorcontrib>Fukuda, Jinichi</creatorcontrib><title>Immunohistochemical study of interleukin-1β and interleukin-1 receptor antagonist in an antigen-induced arthritis of the rabbit temporomandibular joint</title><title>Journal of oral pathology & medicine</title><description>Background: In temporomandibular joint (TMJ) arthritis, there is limited knowledge of the relationship between interleukin‐1β (IL‐1β) and interleukin‐1 receptor antagonist (IL‐1ra), as well as the source of these cytokines. We investigated the development of an antigen‐induced arthritis in the rabbit TMJ immunohistochemically.
Methods: Unilateral TMJ arthritis was induced in 32 adult New Zealand White rabbits. From 6 h to 12 weeks after induction of arthritis, topology of IL‐1β and IL‐1ra were observed.
Result: The acute stage of induced arthritis lasted for one week after induction, thereafter it became chronic. In the early phase of the acute stage, infiltrating inflammatory cells, as well as synovial cells, produced IL‐1β and IL‐1ra. In the late phase of the acute stage, the main source of these cytokines was subsynovial fibroblasts. In this phase of arthritis, IL‐1β and IL‐1ra did not appear to be produced by synovial cells. From the early to intermediate phase of the chronic stage, proliferating synovial cells produced IL‐1β and IL‐1ra. In this phase of the arthritis, these cytokines were also observed in a cluster formation in chondrocytes.
Conclusion: This arthritis model shows a staging of the joint inflammation process with time. IL‐1β and IL‐1ra are produced by a certain kind of cells depending on the stage of inflammation.</description><subject>antigen-induced arthritis</subject><subject>Biological and medical sciences</subject><subject>Diseases of the osteoarticular system</subject><subject>Facial bones, jaws, teeth, parodontium: diseases, semeiology</subject><subject>immunohistochemistry</subject><subject>Inflammatory joint diseases</subject><subject>interleukin-1 receptor antagonist</subject><subject>interleukin-1β</subject><subject>Medical sciences</subject><subject>Non tumoral diseases</subject><subject>Otorhinolaryngology. Stomatology</subject><subject>rabbit</subject><subject>temporomandibular joint</subject><issn>0904-2512</issn><issn>1600-0714</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNqNkU2OFCEYhitGE9vRO7DRXbVQUFC1MmZ0fszEcTHqklDwMU13VdEClem-iefwIJ5Jyu70xJ0r4OXh-ULeokAELwlm_O16iVvMyqom1bLCmOQU12K5e1IsCMe4xIKwp8XiBD0vXsS4zqCgjCyKn9fDMI1-5WLyegWD06pHMU1mj7xFbkwQepg2bizJ719IjebfDAXQsE0-5Kuk7v2YPZnIpzlw9zCWbjSTBoNUSKvgkouzOK0ABdV1LqEEw9YHP2S366ZeBbT2ecbL4plVfYRXx_Ws-Hrx8e78qry5vbw-f39T6hrjpqQCTMuZsdZYaBgw0RFLW1VVndCd0UJXnAFvNbXKmK62jGkOgtSUYdCK07OiPHjjA2ynTm6DG1TYS6-cPEabvANZt0wInPk3B34b_I8JYpKDixr6Xo3gpygr3IiGVLO4OYA6-BgD2JOaYDlXJ9dybkXOrci5Ovm3OrnLT18fZ6iY-7BBjdrFx_e0bngtWObeHbgH18P-v_3y0-0XSjDBzePvc2-wOxlU2EguqKjl98-X8urDN44v7qhk9A_bw8JI</recordid><startdate>200201</startdate><enddate>200201</enddate><creator>Habu, Manabu</creator><creator>Tominaga, Kazuhiro</creator><creator>Sukedai, Miho</creator><creator>Alstergren, Per</creator><creator>Ohkawara, Susumu</creator><creator>Kopp, Sigvard</creator><creator>Fukuda, Jinichi</creator><general>Blackwell Science, Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>200201</creationdate><title>Immunohistochemical study of interleukin-1β and interleukin-1 receptor antagonist in an antigen-induced arthritis of the rabbit temporomandibular joint</title><author>Habu, Manabu ; Tominaga, Kazuhiro ; Sukedai, Miho ; Alstergren, Per ; Ohkawara, Susumu ; Kopp, Sigvard ; Fukuda, Jinichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5008-37ed964dffdfe84e47b1f39a22b7cbdc7c264e69c3faddb5f44c6e715340eca63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>antigen-induced arthritis</topic><topic>Biological and medical sciences</topic><topic>Diseases of the osteoarticular system</topic><topic>Facial bones, jaws, teeth, parodontium: diseases, semeiology</topic><topic>immunohistochemistry</topic><topic>Inflammatory joint diseases</topic><topic>interleukin-1 receptor antagonist</topic><topic>interleukin-1β</topic><topic>Medical sciences</topic><topic>Non tumoral diseases</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>rabbit</topic><topic>temporomandibular joint</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Habu, Manabu</creatorcontrib><creatorcontrib>Tominaga, Kazuhiro</creatorcontrib><creatorcontrib>Sukedai, Miho</creatorcontrib><creatorcontrib>Alstergren, Per</creatorcontrib><creatorcontrib>Ohkawara, Susumu</creatorcontrib><creatorcontrib>Kopp, Sigvard</creatorcontrib><creatorcontrib>Fukuda, Jinichi</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Journal of oral pathology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Habu, Manabu</au><au>Tominaga, Kazuhiro</au><au>Sukedai, Miho</au><au>Alstergren, Per</au><au>Ohkawara, Susumu</au><au>Kopp, Sigvard</au><au>Fukuda, Jinichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunohistochemical study of interleukin-1β and interleukin-1 receptor antagonist in an antigen-induced arthritis of the rabbit temporomandibular joint</atitle><jtitle>Journal of oral pathology & medicine</jtitle><date>2002-01</date><risdate>2002</risdate><volume>31</volume><issue>1</issue><spage>45</spage><epage>54</epage><pages>45-54</pages><issn>0904-2512</issn><eissn>1600-0714</eissn><abstract>Background: In temporomandibular joint (TMJ) arthritis, there is limited knowledge of the relationship between interleukin‐1β (IL‐1β) and interleukin‐1 receptor antagonist (IL‐1ra), as well as the source of these cytokines. We investigated the development of an antigen‐induced arthritis in the rabbit TMJ immunohistochemically.
Methods: Unilateral TMJ arthritis was induced in 32 adult New Zealand White rabbits. From 6 h to 12 weeks after induction of arthritis, topology of IL‐1β and IL‐1ra were observed.
Result: The acute stage of induced arthritis lasted for one week after induction, thereafter it became chronic. In the early phase of the acute stage, infiltrating inflammatory cells, as well as synovial cells, produced IL‐1β and IL‐1ra. In the late phase of the acute stage, the main source of these cytokines was subsynovial fibroblasts. In this phase of arthritis, IL‐1β and IL‐1ra did not appear to be produced by synovial cells. From the early to intermediate phase of the chronic stage, proliferating synovial cells produced IL‐1β and IL‐1ra. In this phase of the arthritis, these cytokines were also observed in a cluster formation in chondrocytes.
Conclusion: This arthritis model shows a staging of the joint inflammation process with time. IL‐1β and IL‐1ra are produced by a certain kind of cells depending on the stage of inflammation.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science, Ltd</pub><doi>10.1046/j.0904-2512.2001.10057.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | antigen-induced arthritis Biological and medical sciences Diseases of the osteoarticular system Facial bones, jaws, teeth, parodontium: diseases, semeiology immunohistochemistry Inflammatory joint diseases interleukin-1 receptor antagonist interleukin-1β Medical sciences Non tumoral diseases Otorhinolaryngology. Stomatology rabbit temporomandibular joint |
| title | Immunohistochemical study of interleukin-1β and interleukin-1 receptor antagonist in an antigen-induced arthritis of the rabbit temporomandibular joint |
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