Suppression of interleukin-10 release from human periodontal ligament cells by interleukin-1 beta in vitro

Citation
J. Deschner et al., Suppression of interleukin-10 release from human periodontal ligament cells by interleukin-1 beta in vitro, ARCH ORAL B, 45(2), 2000, pp. 179-183
Citations number
28
Language
INGLESE
art.tipo
Article
Categorie Soggetti
da verificare
Journal title
ARCHIVES OF ORAL BIOLOGY
ISSN journal
0003-9969 → ACNP
Volume
45
Issue
2
Year of publication
2000
Pages
179 - 183
Database
ISI
SICI code
0003-9969(200002)45:2<179:SOIRFH>2.0.ZU;2-3
Abstract
Periodontitis is characterized by an inflammatory process induced by period ontopathogenic bacteria in the subgingival plaque. Periodontal inflammation can be enhanced by both an increase of inflammatory stimulators, e.g. inte rleukin (IL)-6, and a decrease of inflammatory inhibitors, e.g. IL-10. The amount of IL-1 beta is known to be increased in gingival tissues and in the gingival crevicular fluid from inflamed sites compared to healthy sites. T his in vitro study sought to clarify whether IL-1 beta (1 ng/ml) has a regu latory effect on the release of these two cytokines from human periodontal ligament (PDL) cells. PDL cells derived fi om healthy premolars were grown in the presence and absence (control) of IL-1 beta. The concentration of IL -6 and IL-10 in the supernatants was assessed by enzyme-linked immunosorben t assay after 48 h of culture. PDL cells incubated with IL-1 beta released significantly (p 0.05) higher amounts of IL-6 and significantly (p < 0.01) smaller amounts of IL-10 compared to control. These results give further su pport to the observation that IL-1 beta can increase the IL-6 secretion fro m PDL cells. Moreover, they provide original evidence that PDL cells secret e IL-10, which can be suppressed by IL-1 beta. It is concluded that PDL cel ls can function as accessory immunoinflammatory cells amplifying the inflam matory process in periodontitis and. thereby, contributing to periodontal b reakdown. (C) 2000 Elsevier Science Ltd. All rights reserved.