Assessment of the involvement of the macrophage migration inhibitory factor–glucocorticoid regulatory dyad in the expression of matrix metalloproteinase‐2 during periodontitis
Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine and counter‐regulator of endogenous glucocorticoids (GCs). It is implicated in acute and chronic inflammatory diseases. This study investigated the role of the MIF–GC regulatory dyad in the expression and release of matrix me...
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Veröffentlicht in: | European journal of oral sciences 2017-10, Vol.125 (5), p.345-354 |
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creator | Hirschfeld, Josefine Howait, Mohammed Movila, Alexandru Parčina, Marijo Bekeredjian‐Ding, Isabelle Deschner, James Jepsen, Søren Kawai, Toshihisa |
description | Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine and counter‐regulator of endogenous glucocorticoids (GCs). It is implicated in acute and chronic inflammatory diseases. This study investigated the role of the MIF–GC regulatory dyad in the expression and release of matrix metalloproteinase‐2 (MMP‐2) during periodontitis, in vivo and in vitro. In a Mif‐knockout (KO) mouse model of ligature‐induced periodontitis, gingival tissues and blood were collected and analysed for levels of interleukin‐6 (IL‐6), MIF, MMP‐2, and corticosterone. In addition, human gingival fibroblasts (HGFs) were tested for production of IL‐6 and MMP‐2 after stimulation with hydrocortisone (HC), MIF, tumour necrosis factor‐alpha (TNF‐α), or Fusobacterium nucleatum, a pathogen known to elicit immune responses during periodontitis. Wild‐type (WT) mice showed a local and systemic increase of MIF levels during inflammation, which was confirmed by increased local IL‐6 concentrations. Systemic GC levels were reduced in WT and Mif‐KO mice during inflammation, with overall lower concentrations in Mif‐KO mice. In vivo and in vitro, MMP‐2 production was not dependent on MIF or inflammatory stimuli, but was inhibited by HC. Therefore, MIF does not appear to stimulate expression of MMP‐2 in the gingival tissues, whereas GC upregulates MIF and downregulates MMP‐2. Our findings further suggest that MIF may regulate systemic GC levels. |
doi_str_mv | 10.1111/eos.12363 |
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It is implicated in acute and chronic inflammatory diseases. This study investigated the role of the MIF–GC regulatory dyad in the expression and release of matrix metalloproteinase‐2 (MMP‐2) during periodontitis, in vivo and in vitro. In a Mif‐knockout (KO) mouse model of ligature‐induced periodontitis, gingival tissues and blood were collected and analysed for levels of interleukin‐6 (IL‐6), MIF, MMP‐2, and corticosterone. In addition, human gingival fibroblasts (HGFs) were tested for production of IL‐6 and MMP‐2 after stimulation with hydrocortisone (HC), MIF, tumour necrosis factor‐alpha (TNF‐α), or Fusobacterium nucleatum, a pathogen known to elicit immune responses during periodontitis. Wild‐type (WT) mice showed a local and systemic increase of MIF levels during inflammation, which was confirmed by increased local IL‐6 concentrations. Systemic GC levels were reduced in WT and Mif‐KO mice during inflammation, with overall lower concentrations in Mif‐KO mice. In vivo and in vitro, MMP‐2 production was not dependent on MIF or inflammatory stimuli, but was inhibited by HC. Therefore, MIF does not appear to stimulate expression of MMP‐2 in the gingival tissues, whereas GC upregulates MIF and downregulates MMP‐2. Our findings further suggest that MIF may regulate systemic GC levels.</description><identifier>ISSN: 0909-8836</identifier><identifier>EISSN: 1600-0722</identifier><identifier>DOI: 10.1111/eos.12363</identifier><identifier>PMID: 28776753</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Animal tissues ; Animals ; Cells, Cultured ; Corticosterone ; Corticosterone - pharmacology ; cytokines ; Dentistry ; Enzyme-Linked Immunosorbent Assay ; Fibroblasts ; Fibroblasts - metabolism ; Fusobacterium nucleatum - pathogenicity ; Gelatinase A ; Gingiva ; Glucocorticoids ; Gum disease ; Humans ; Hydrocortisone ; Hydrocortisone - pharmacology ; Immune response ; In vitro methods and tests ; inflammation ; Inflammatory diseases ; Interleukin 6 ; Interleukin-6 - metabolism ; Interleukins ; knockout ; Leukocyte migration ; Macrophage migration inhibitory factor ; Macrophage Migration-Inhibitory Factors - pharmacology ; Macrophages ; Matrix metalloproteinase ; Matrix Metalloproteinase 2 - metabolism ; matrixmetalloproteinases ; Metalloproteinase ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Periodontitis ; Periodontitis - metabolism ; Polymerase Chain Reaction ; Rodents ; Stimulation ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factor-TNF ; Tumors</subject><ispartof>European journal of oral sciences, 2017-10, Vol.125 (5), p.345-354</ispartof><rights>2017 Eur J Oral Sci</rights><rights>2017 Eur J Oral Sci.</rights><rights>Copyright © 2017 European Journal of Oral Sciences</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4543-135a2a8f465f4804bdfd90aa9c8acf1ea87be99948b6a72e8d84ca5a5c1638fb3</citedby><cites>FETCH-LOGICAL-c4543-135a2a8f465f4804bdfd90aa9c8acf1ea87be99948b6a72e8d84ca5a5c1638fb3</cites><orcidid>0000-0001-8512-7411</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Feos.12363$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Feos.12363$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28776753$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hirschfeld, Josefine</creatorcontrib><creatorcontrib>Howait, Mohammed</creatorcontrib><creatorcontrib>Movila, Alexandru</creatorcontrib><creatorcontrib>Parčina, Marijo</creatorcontrib><creatorcontrib>Bekeredjian‐Ding, Isabelle</creatorcontrib><creatorcontrib>Deschner, James</creatorcontrib><creatorcontrib>Jepsen, Søren</creatorcontrib><creatorcontrib>Kawai, Toshihisa</creatorcontrib><title>Assessment of the involvement of the macrophage migration inhibitory factor–glucocorticoid regulatory dyad in the expression of matrix metalloproteinase‐2 during periodontitis</title><title>European journal of oral sciences</title><addtitle>Eur J Oral Sci</addtitle><description>Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine and counter‐regulator of endogenous glucocorticoids (GCs). It is implicated in acute and chronic inflammatory diseases. This study investigated the role of the MIF–GC regulatory dyad in the expression and release of matrix metalloproteinase‐2 (MMP‐2) during periodontitis, in vivo and in vitro. In a Mif‐knockout (KO) mouse model of ligature‐induced periodontitis, gingival tissues and blood were collected and analysed for levels of interleukin‐6 (IL‐6), MIF, MMP‐2, and corticosterone. In addition, human gingival fibroblasts (HGFs) were tested for production of IL‐6 and MMP‐2 after stimulation with hydrocortisone (HC), MIF, tumour necrosis factor‐alpha (TNF‐α), or Fusobacterium nucleatum, a pathogen known to elicit immune responses during periodontitis. Wild‐type (WT) mice showed a local and systemic increase of MIF levels during inflammation, which was confirmed by increased local IL‐6 concentrations. Systemic GC levels were reduced in WT and Mif‐KO mice during inflammation, with overall lower concentrations in Mif‐KO mice. In vivo and in vitro, MMP‐2 production was not dependent on MIF or inflammatory stimuli, but was inhibited by HC. Therefore, MIF does not appear to stimulate expression of MMP‐2 in the gingival tissues, whereas GC upregulates MIF and downregulates MMP‐2. Our findings further suggest that MIF may regulate systemic GC levels.</description><subject>Animal tissues</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Corticosterone</subject><subject>Corticosterone - pharmacology</subject><subject>cytokines</subject><subject>Dentistry</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fusobacterium nucleatum - pathogenicity</subject><subject>Gelatinase A</subject><subject>Gingiva</subject><subject>Glucocorticoids</subject><subject>Gum disease</subject><subject>Humans</subject><subject>Hydrocortisone</subject><subject>Hydrocortisone - pharmacology</subject><subject>Immune response</subject><subject>In vitro methods and tests</subject><subject>inflammation</subject><subject>Inflammatory diseases</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Interleukins</subject><subject>knockout</subject><subject>Leukocyte migration</subject><subject>Macrophage migration inhibitory factor</subject><subject>Macrophage Migration-Inhibitory Factors - pharmacology</subject><subject>Macrophages</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>matrixmetalloproteinases</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Periodontitis</subject><subject>Periodontitis - metabolism</subject><subject>Polymerase Chain Reaction</subject><subject>Rodents</subject><subject>Stimulation</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumors</subject><issn>0909-8836</issn><issn>1600-0722</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAQxy1ERZdtD7wAisQFDmn9Fcc5VlX5kCr1AJyjiTPJukriYDule-sjIPEovFGfBHe3RQgJX8ayfv7NaP6EvGL0hKVzii6cMC6UeEZWTFGa05Lz52RFK1rlWgt1SF6GcE0pE6wqX5BDrstSlYVYkV9nIWAII04xc10WN5jZ6cYNN_j30wjGu3kDfbra3kO0bkrcxjY2Or_NOjCp3t_97IfFOON8tMbZNvPYLwPskHYLbfqy0-Ht7FPTB0lqMEL09jYbMcIwuNm7iHaCgPd3P3jWLt5OfTajt651U7TRhiNy0MEQ8PixrsnX9xdfzj_ml1cfPp2fXeZGFlLkTBTAQXdSFZ3UVDZt11YUoDIaTMcQdNlgVVVSNwpKjrrV0kABhWFK6K4Ra_J2700zfVswxHq0weAwwIRuCTWruFJa8rTINXnzD3rtFj-l6RIlCi5kwWWi3u2ptM0QPHb17O0IflszWj8kWack612SiX39aFyaEds_5FN0CTjdA9_tgNv_m-qLq8975W_d56_y</recordid><startdate>201710</startdate><enddate>201710</enddate><creator>Hirschfeld, Josefine</creator><creator>Howait, Mohammed</creator><creator>Movila, Alexandru</creator><creator>Parčina, Marijo</creator><creator>Bekeredjian‐Ding, Isabelle</creator><creator>Deschner, James</creator><creator>Jepsen, Søren</creator><creator>Kawai, Toshihisa</creator><general>Wiley Subscription Services, 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>7QO</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8512-7411</orcidid></search><sort><creationdate>201710</creationdate><title>Assessment of the involvement of the macrophage migration inhibitory factor–glucocorticoid regulatory dyad in the expression of matrix metalloproteinase‐2 during periodontitis</title><author>Hirschfeld, Josefine ; Howait, Mohammed ; Movila, Alexandru ; Parčina, Marijo ; Bekeredjian‐Ding, Isabelle ; Deschner, James ; Jepsen, Søren ; Kawai, Toshihisa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4543-135a2a8f465f4804bdfd90aa9c8acf1ea87be99948b6a72e8d84ca5a5c1638fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animal tissues</topic><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Corticosterone</topic><topic>Corticosterone - pharmacology</topic><topic>cytokines</topic><topic>Dentistry</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Fusobacterium nucleatum - pathogenicity</topic><topic>Gelatinase A</topic><topic>Gingiva</topic><topic>Glucocorticoids</topic><topic>Gum disease</topic><topic>Humans</topic><topic>Hydrocortisone</topic><topic>Hydrocortisone - pharmacology</topic><topic>Immune response</topic><topic>In vitro methods and tests</topic><topic>inflammation</topic><topic>Inflammatory diseases</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>Interleukins</topic><topic>knockout</topic><topic>Leukocyte migration</topic><topic>Macrophage migration inhibitory factor</topic><topic>Macrophage Migration-Inhibitory Factors - pharmacology</topic><topic>Macrophages</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>matrixmetalloproteinases</topic><topic>Metalloproteinase</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Periodontitis</topic><topic>Periodontitis - metabolism</topic><topic>Polymerase Chain Reaction</topic><topic>Rodents</topic><topic>Stimulation</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hirschfeld, Josefine</creatorcontrib><creatorcontrib>Howait, Mohammed</creatorcontrib><creatorcontrib>Movila, Alexandru</creatorcontrib><creatorcontrib>Parčina, Marijo</creatorcontrib><creatorcontrib>Bekeredjian‐Ding, Isabelle</creatorcontrib><creatorcontrib>Deschner, James</creatorcontrib><creatorcontrib>Jepsen, Søren</creatorcontrib><creatorcontrib>Kawai, Toshihisa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of oral sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hirschfeld, Josefine</au><au>Howait, Mohammed</au><au>Movila, Alexandru</au><au>Parčina, Marijo</au><au>Bekeredjian‐Ding, Isabelle</au><au>Deschner, James</au><au>Jepsen, Søren</au><au>Kawai, Toshihisa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Assessment of the involvement of the macrophage migration inhibitory factor–glucocorticoid regulatory dyad in the expression of matrix metalloproteinase‐2 during periodontitis</atitle><jtitle>European journal of oral sciences</jtitle><addtitle>Eur J Oral Sci</addtitle><date>2017-10</date><risdate>2017</risdate><volume>125</volume><issue>5</issue><spage>345</spage><epage>354</epage><pages>345-354</pages><issn>0909-8836</issn><eissn>1600-0722</eissn><abstract>Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine and counter‐regulator of endogenous glucocorticoids (GCs). It is implicated in acute and chronic inflammatory diseases. This study investigated the role of the MIF–GC regulatory dyad in the expression and release of matrix metalloproteinase‐2 (MMP‐2) during periodontitis, in vivo and in vitro. In a Mif‐knockout (KO) mouse model of ligature‐induced periodontitis, gingival tissues and blood were collected and analysed for levels of interleukin‐6 (IL‐6), MIF, MMP‐2, and corticosterone. In addition, human gingival fibroblasts (HGFs) were tested for production of IL‐6 and MMP‐2 after stimulation with hydrocortisone (HC), MIF, tumour necrosis factor‐alpha (TNF‐α), or Fusobacterium nucleatum, a pathogen known to elicit immune responses during periodontitis. Wild‐type (WT) mice showed a local and systemic increase of MIF levels during inflammation, which was confirmed by increased local IL‐6 concentrations. Systemic GC levels were reduced in WT and Mif‐KO mice during inflammation, with overall lower concentrations in Mif‐KO mice. In vivo and in vitro, MMP‐2 production was not dependent on MIF or inflammatory stimuli, but was inhibited by HC. Therefore, MIF does not appear to stimulate expression of MMP‐2 in the gingival tissues, whereas GC upregulates MIF and downregulates MMP‐2. Our findings further suggest that MIF may regulate systemic GC levels.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28776753</pmid><doi>10.1111/eos.12363</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-8512-7411</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animal tissues Animals Cells, Cultured Corticosterone Corticosterone - pharmacology cytokines Dentistry Enzyme-Linked Immunosorbent Assay Fibroblasts Fibroblasts - metabolism Fusobacterium nucleatum - pathogenicity Gelatinase A Gingiva Glucocorticoids Gum disease Humans Hydrocortisone Hydrocortisone - pharmacology Immune response In vitro methods and tests inflammation Inflammatory diseases Interleukin 6 Interleukin-6 - metabolism Interleukins knockout Leukocyte migration Macrophage migration inhibitory factor Macrophage Migration-Inhibitory Factors - pharmacology Macrophages Matrix metalloproteinase Matrix Metalloproteinase 2 - metabolism matrixmetalloproteinases Metalloproteinase Mice Mice, Inbred C57BL Mice, Knockout Periodontitis Periodontitis - metabolism Polymerase Chain Reaction Rodents Stimulation Tumor necrosis factor Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-TNF Tumors |
title | Assessment of the involvement of the macrophage migration inhibitory factor–glucocorticoid regulatory dyad in the expression of matrix metalloproteinase‐2 during periodontitis |
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