Triclosan reduces prostaglandin biosynthesis in human gingival fibroblasts challenged with interleukin-1 in vitro.
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-1beta (IL-1beta) or tumor necrosis factor alpha (TNFalpha) was studied in vitro. When gingival fibroblasts were treated simultaneously with triclosan and IL-1beta, the stimulatory effect of IL-1beta on prostaglandin E2 (PGE2) and PGI2 formation was reduced in a dose-dependent manner by triclosan. Triclosan also reduced the PGE2 formation induced by TNFalpha. Furthermore, the capacity of IL-1beta 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-1beta, was markedly reduced in the presence of triclosan. The study indicates that the stimulatory effect of IL-1beta on prostanoid formation (PGE2, PGI2) in human gingival fibroblasts was diminished in the presence of triclosan 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.
Modéer
T
T
Department of Pediatric Dentistry, Faculty of Odontology, Karolinska Institutet, Huddinge, Sweden.
Bengtsson
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A
Rölla
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G
D000328:Adult; D000891:Anti-Infective Agents, Local / Q000008:administration & dosage / Q000494:pharmacology*; D001095:Arachidonic Acids / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000493:pharmacokinetics; D002478:Cells, Cultured; D002648:Child; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D005881:Gingiva / Q000187:drug effects* / Q000378:metabolism; D005891:Gingivitis / Q000188:drug therapy; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors / Q000378:metabolism; D007375:Interleukin-1 / Q000008:administration & dosage / Q000494:pharmacology*; D010741:Phospholipases A / Q000037:antagonists & inhibitors; D054467:Phospholipases A2; D019275:Radiopharmaceuticals; D014260:Triclosan / Q000008:administration & dosage / Q000494:pharmacology*; D014316:Tritium; D014409:Tumor Necrosis Factor-alpha / Q000008:administration & dosage / Q000494:pharmacology; D015854:Up-Regulation / Q000187:drug effects
D000891:Anti-Infective Agents, Local; D001095:Arachidonic Acids; D016861:Cyclooxygenase Inhibitors; D018836:Inflammation Mediators; D007375:Interleukin-1; D019275:Radiopharmaceuticals; D014409:Tumor Necrosis Factor-alpha; D014316:Tritium; D014260:Triclosan; D011464:Epoprostenol; D010741:Phospholipases A; D054467:Phospholipases A2; D015232:Dinoprostone