Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro
Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treat...
Ausführliche Beschreibung
Autor*in: |
Modéer, T. [verfasserIn] Bengisson, A. [verfasserIn] Rölla, G. [verfasserIn] |
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E-Artikel |
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Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1996 |
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Online-Ressource |
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Reproduktion: |
2005 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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Übergeordnetes Werk: |
In: Journal of clinical periodontology - Oxford [u.a.] : Wiley-Blackwell, 1974, 23(1996), 10, Seite 0 |
Übergeordnetes Werk: |
volume:23 ; year:1996 ; number:10 ; pages:0 |
Links: |
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DOI / URN: |
10.1111/j.1600-051X.1996.tb00513.x |
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520 | |a Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. | ||
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10.1111/j.1600-051X.1996.tb00513.x doi (DE-627)NLEJ240714571 DE-627 ger DE-627 rakwb Modéer, T. verfasserin aut Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro Oxford, UK Blackwell Publishing Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| gingival fibroblasts Bengisson, A. verfasserin aut Rölla, G. verfasserin aut In Journal of clinical periodontology Oxford [u.a.] : Wiley-Blackwell, 1974 23(1996), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927142 (DE-600)2026349-1 1600-051X nnns volume:23 year:1996 number:10 pages:0 http://dx.doi.org/10.1111/j.1600-051X.1996.tb00513.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1996 10 0 |
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10.1111/j.1600-051X.1996.tb00513.x doi (DE-627)NLEJ240714571 DE-627 ger DE-627 rakwb Modéer, T. verfasserin aut Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro Oxford, UK Blackwell Publishing Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| gingival fibroblasts Bengisson, A. verfasserin aut Rölla, G. verfasserin aut In Journal of clinical periodontology Oxford [u.a.] : Wiley-Blackwell, 1974 23(1996), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927142 (DE-600)2026349-1 1600-051X nnns volume:23 year:1996 number:10 pages:0 http://dx.doi.org/10.1111/j.1600-051X.1996.tb00513.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1996 10 0 |
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10.1111/j.1600-051X.1996.tb00513.x doi (DE-627)NLEJ240714571 DE-627 ger DE-627 rakwb Modéer, T. verfasserin aut Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro Oxford, UK Blackwell Publishing Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| gingival fibroblasts Bengisson, A. verfasserin aut Rölla, G. verfasserin aut In Journal of clinical periodontology Oxford [u.a.] : Wiley-Blackwell, 1974 23(1996), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927142 (DE-600)2026349-1 1600-051X nnns volume:23 year:1996 number:10 pages:0 http://dx.doi.org/10.1111/j.1600-051X.1996.tb00513.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1996 10 0 |
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10.1111/j.1600-051X.1996.tb00513.x doi (DE-627)NLEJ240714571 DE-627 ger DE-627 rakwb Modéer, T. verfasserin aut Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro Oxford, UK Blackwell Publishing Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| gingival fibroblasts Bengisson, A. verfasserin aut Rölla, G. verfasserin aut In Journal of clinical periodontology Oxford [u.a.] : Wiley-Blackwell, 1974 23(1996), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927142 (DE-600)2026349-1 1600-051X nnns volume:23 year:1996 number:10 pages:0 http://dx.doi.org/10.1111/j.1600-051X.1996.tb00513.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1996 10 0 |
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10.1111/j.1600-051X.1996.tb00513.x doi (DE-627)NLEJ240714571 DE-627 ger DE-627 rakwb Modéer, T. verfasserin aut Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro Oxford, UK Blackwell Publishing Ltd 1996 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| gingival fibroblasts Bengisson, A. verfasserin aut Rölla, G. verfasserin aut In Journal of clinical periodontology Oxford [u.a.] : Wiley-Blackwell, 1974 23(1996), 10, Seite 0 Online-Ressource (DE-627)NLEJ243927142 (DE-600)2026349-1 1600-051X nnns volume:23 year:1996 number:10 pages:0 http://dx.doi.org/10.1111/j.1600-051X.1996.tb00513.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 23 1996 10 0 |
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Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. |
abstractGer |
Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. |
abstract_unstemmed |
Abstract The effect of the toothpaste ingredient triclosan (2,4,4′-trichloro-2′-hydroxyldiphenyl ether) on the prostaglandins biosynthesis in human gingival fibroblasts challenged with interleukin-1β (IL-1β) or tumor necrosis factor α (TNFα) was studied in vitro. When gingival fibroblasts were treated simultaneously with triciosan and IL-1β, the stimulatory effect of IL-1β on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE: formation induced by TNFα. Furthermore, the capacity of IL-1β to induce release of [3H] arachidonic acid from prelabelled gingival fibroblasts was reduced in the presence of triclosan. Addition of exogenous unlabelled arachidonic acid (AA) to the cells resulted in enhanced PGE2 formation which was reduced by triclosan. The upregulation of the metabolism of AA to PGE2 induced by IL-lβ, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1β on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triciosan partly at the level of phospholipase A2 and partly at the level of cyclooxygenase. The present data that triclosan. in vitro, inhibits the production of inflammatory mediators such as prostaglandins suggests that this can be an aspect of its clinical effect on gingivitis, in addition to its antibacterial effect. |
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title_short |
Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro |
url |
http://dx.doi.org/10.1111/j.1600-051X.1996.tb00513.x |
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Bengisson, A. Rölla, G. |
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10.1111/j.1600-051X.1996.tb00513.x |
up_date |
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