Interleukin-11 production in gingival fibroblasts stimulated with lipopolysaccharides and IL-1a

Objectives: Interleukin-11 (IL-11) and IL-6 augment the expression of receptor activator of NF kappa B ligand (RANKL) in osteoblasts and enhance the osteoclast differentiation. Inflammatory mediators, including lipopolysaccharides (LPS) and IL-1a, stimulate human gingival fibroblast (HGF) to produce IL-6, but little is known about IL-11. To understand what role IL-11 plays in periodontal disease, production of IL-11 in HGF stimulated with LPS, IL-1a was examined. Methods: HGFs were stimulated with LPS, IL-1a respectively. The production of IL-11 and IL-6 was measured using enzyme-linked immunosorbent assay (ELISA). IL-11 and Glyceraldehyde 3 ¨CPhosphate Dehydrogenase (GAPDH) messenger RNA (mRNA) levels in HGF were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). Results: LPS from Escherichia coli (E.coli), Actinobacillus actinomycetemcomitans (A.a.) and Porphyromonas gingivalis (P.g.), and IL-1a significantly increased both production levels of IL-11 and IL-6 in HGF. Indomethacin significantly reduced IL-11 and IL-6 production by LPS-stimulated HGF. Meanwhile, the addition of indomethacin also resulted in significant suppression of IL-11 production by IL-1a-stimulated HGF. However, IL-6 production, which was significantly suppressed or slightly enhanced, was regulated by indomethacin differently in IL-1a-stimulated HGF. IL-1a enhanced the ratio of IL-11/GAPDH mRNA expression in HGF, and the augmentation was abolished by indomethacin. Conclusions: Production of IL-11 in HGF stimulated with IL-1a was transcriptionally upregulated by the endogenous prostaglandin synthesis. And endogenous prostaglandin also upregulated production of IL-11 / IL-6 in LPSs- stimulated HGF. Inhibition of prostaglandin might suppress the osteoclastogenesis by IL-11 in inflammatory periodontal diseases.