Enhanced cyclooxygenase-2 mRNA expression in human gingival fibroblasts induced by cell contact with human lymphocytes.
Prostaglandins, especially prostaglandin E2 (PGE2), play a crucial role in the pathogenesis of periodontal disease. We have previously reported that inflammatory mediators interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha) increase the production of PGE2 in human gingival fibroblasts. In this study, we investigated the effect of cell-to-cell interactions between gingival fibroblasts and lymphocytes on PGE2 production by using co-culture technique. Cell-to-cell contact between gingival fibroblasts and lymphocytes synergistically enhanced the production of PGE2 in co-cultures. In contrast to lymphocytes, the cyclooxygenase-2 (COX-2) mRNA expression in gingival fibroblasts was strongly enhanced following cell contact between gingival fibroblasts and lymphocytes. The level of COX-1 mRNA expression, however, was not affected either in gingival fibroblasts or in lymphocytes by the interactions between fibroblasts and lymphocytes. The study demonstrates that cell contact between gingival fibroblasts and lymphocytes strongly stimulates PGE2 production partly due to enhanced COX-2 mRNA expression in gingival fibroblasts. The cell-to-cell contact between gingival fibroblasts and lymphocytes should be considered as an important regulatory aspect for the enhancement of PGE2 in periodontal disease.
Yucel-Lindberg
T
T
Department of Pediatric Dentistry, Karolinska Institutet, Huddinge, Sweden. tulay.lindberg@ofa.ki.se
Brunius
G
G
Wondimu
B
B
Andurén
I
I
Modéer
T
T
D002450:Cell Communication; D002452:Cell Count; D018929:Cell Culture Techniques; D018920:Coculture Techniques; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D005347:Fibroblasts / Q000378:metabolism* / Q000502:physiology; D015971:Gene Expression Regulation, Enzymologic; D005881:Gingiva / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000235:genetics*; D008214:Lymphocytes / Q000502:physiology*; D008565:Membrane Proteins; D009578:Nitrobenzenes / Q000494:pharmacology; D010510:Periodontal Diseases / Q000201:enzymology / Q000378:metabolism; D010544:Peroxidases / Q000037:antagonists & inhibitors / Q000235:genetics*; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics*; D013223:Statistics as Topic; D013449:Sulfonamides / Q000494:pharmacology; D015854:Up-Regulation
D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D009578:Nitrobenzenes; D012333:RNA, Messenger; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D010544:Peroxidases; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496511:PTGS1 protein, human; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone