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
Hauptverfasser: Hirschfeld, Josefine, Howait, Mohammed, Movila, Alexandru, Parčina, Marijo, Bekeredjian‐Ding, Isabelle, Deschner, James, Jepsen, Søren, Kawai, Toshihisa
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container_end_page 354
container_issue 5
container_start_page 345
container_title European journal of oral sciences
container_volume 125
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.</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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