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
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.