Ca. Czuszak et al., PROSTAGLANDIN E(2) POTENTIATES INTERLEUKIN-1-BETA INDUCED INTERLEUKIN-6 PRODUCTION BY HUMAN GINGIVAL FIBROBLASTS, Journal of clinical periodontology, 23(7), 1996, pp. 635-640
Increased levels of cytokines and prostanoids have been detected in in
flamed gingival tissue and may play an important role in periodontal p
athogenesis. Recent studies suggest that monocytic products, such as i
nterleukin (IL)-1 beta, could stimulate IL-6 production by human gingi
val fibroblasts (HGF). In this context, the production of local cytoki
nes and inflammatory mediators could regulate the secretory capacity o
f resident gingival fibroblasts. Therefore, the purpose of this study
was to determine if PGE(2) induced by IL-1 beta could potentiate the I
L-6 response by HGF. Utilizing an ELISA, it was determined that maxima
l IL-6 occurred when HGF were stimulated with 0.10-10 nM IL-1 beta. Th
ese concentrations of IL-1 beta also induced a small, but significant
increase in PGE(2) production by HGF. Interestingly, the combination o
f IL gamma beta and PGE(2) induced a synergistic rise in IL-6 producti
on by HGF. Moreover, inclusion of indomethacin caused a 20% reduction
in IL-6 production and totally eliminated PGE(2) production. These fin
dings provide additional rationale for the clinical use of NSAIDs in t
he management of periodontal disease due to their ability to attenuate
production of both PGE(2), and IL-6. These results suggest the endoge
nous PGE(2) induced by IL-1 beta plays an important regulatory role in
IL 6 production by HGF. Moreover, they support the concept that eleva
ted PGE(2)induced during inflammation can regulate HGF secretory funct
ion.