Production of interleukin-11 in human gingival fibroblasts stimulated with IL-1alpha and tumor necrosis factor-alpha.
- Author:
Lu HE
1
;
T NAGASAWA
;
I ISHIKAWA
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Cyclooxygenase Inhibitors; pharmacology; Fibroblasts; drug effects; metabolism; Gingiva; cytology; metabolism; Humans; Indomethacin; pharmacology; Interleukin-11; biosynthesis; Interleukin-1alpha; pharmacology; RNA, Messenger; biosynthesis; Tumor Necrosis Factor-alpha; pharmacology
- From: Chinese Journal of Stomatology 2004;39(6):488-491
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODSHGFs 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).
RESULTSIL-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.
CONCLUSIONSProduction 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.
