Lu He1, T Nagasawa, I Ishikawa. 1. Department of Periodontology, Peking University School of Stomatology, Beijing 100081, China. helu-bj@hotmail.com
Abstract
OBJECTIVE: To investigate what role IL-11 plays in periodontal disease and to determine the level of IL-11 in HGFs stimulated with IL-1alpha and TNF-alpha. METHODS: HGFs were stimulated with IL-1alpha and TNF-alpha alone or in combination. The production of IL-11 was measured using enzyme-linked immunosorbent assay (ELISA). IL-11 and Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH) messenger RNA (mRNA) levels in HGFs were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: IL-1alpha significantly increased the levels of IL-11 in HGFs. TNF-alpha also significantly augmented IL-11 production in HGFs, and synergistically stimulated HGFs to produce IL-11 when combined with IL-1alpha. Indomethacin, an inhibitor of prostaglandin synthesis, significantly reduced IL-11 production by HGFs stimulated with IL-1alpha and TNF-alpha individually or in combination. IL-1alpha alone or combined with TNF-alpha enhanced the ratio of IL-11/GAPDH mRNA expression in HGFs, and the augmentation was abolished by indomethacin after co-incubation for 24 hs. CONCLUSIONS: Production of IL-11 in HGFs stimulated with IL-1alpha and TNF-alpha was transcriptionally upregulated by the endogenous prostaglandin synthesis. Inhibition of prostaglandin might suppress the osteoclastogenesis by IL-11 in inflammatory periodontal diseases.
OBJECTIVE: To investigate what role IL-11 plays in periodontal disease and to determine the level of IL-11 in HGFs stimulated with IL-1alpha and TNF-alpha. METHODS: HGFs were stimulated with IL-1alpha and TNF-alpha alone or in combination. The production of IL-11 was measured using enzyme-linked immunosorbent assay (ELISA). IL-11 and Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH) messenger RNA (mRNA) levels in HGFs were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS:IL-1alpha significantly increased the levels of IL-11 in HGFs. TNF-alpha also significantly augmented IL-11 production in HGFs, and synergistically stimulated HGFs to produce IL-11 when combined with IL-1alpha. Indomethacin, an inhibitor of prostaglandin synthesis, significantly reduced IL-11 production by HGFs stimulated with IL-1alpha and TNF-alpha individually or in combination. IL-1alpha alone or combined with TNF-alpha enhanced the ratio of IL-11/GAPDH mRNA expression in HGFs, and the augmentation was abolished by indomethacin after co-incubation for 24 hs. CONCLUSIONS: Production of IL-11 in HGFs stimulated with IL-1alpha and TNF-alpha was transcriptionally upregulated by the endogenous prostaglandin synthesis. Inhibition of prostaglandin might suppress the osteoclastogenesis by IL-11 in inflammatory periodontal diseases.