RRC ID 19227
著者 Zhang F, Koyama Y, Sanuki R, Mitsui N, Suzuki N, Kimura A, Nakajima A, Shimizu N, Maeno M.
タイトル IL-17A stimulates the expression of inflammatory cytokines via celecoxib-blocked prostaglandin in MC3T3-E1 cells.
ジャーナル Arch Oral Biol
Abstract OBJECTIVE:The prostaglandins (PGs) released from osteoblasts can alter the process of bone remodelling. Recently, we showed that compressive force induced the expression of pro-inflammatory cytokine interleukin (IL)-17s and their receptors in osteoblastic MC3T3-E1 cells and that IL-17A was expressed most highly. Consequently, in the current study we examined the effect of IL-17A and/or celecoxib on PGE(2) production and the expression of cyclooxygenases (COXs) and inflammatory cytokines in MC3T3-E1 cells. We also examined the effects of PGE(2) and cyclohexamide on the expression of inflammatory cytokines.
METHODS:Cells were cultured with or without IL-17A (0.1, 1.0, or 10 ng/ml) in the presence or absence of 10 microM celecoxib, a specific inhibitor of COX-2, for up to 72 h. Cells were pretreated with or without 10 microg/ml cycloheximide, protein synthesis inhibitor, for 30 min, and then cultured with 10 ng/ml IL-17A for 24 h. Cells were also cultured with or without 1.5 ng/ml PGE(2) for 24 h. PGE(2) production was determined by ELISA. The expression of COX-1, COX-2, IL-1alpha, IL-6, IL-8, IL-11, and TNF-alpha mRNAs and proteins was determined by real-time PCR and ELISA, respectively.
RESULTS:The expression of COX-2, IL-1alpha, IL-6, IL-8, IL-11, and TNF-alpha, as well as PGE(2) production increased in the presence of IL-17A, whereas COX-1 expression did not change. Celecoxib blocked the stimulatory effect of IL-17A on the expression of COX-2, IL-1alpha, IL-6, IL-8, and IL-11 as well as PGE(2) production, whereas it did not block TNF-alpha expression. Cycloheximide pretreatment suppressed the expression of IL-17-induced inflammatory cytokines. The expression of IL-1alpha, IL-6, IL-8, and IL-11 increased by the addition of PGE(2), whereas TNF-alpha expression was not affected.
CONCLUSION:These results suggest that IL-17A stimulates the expression of bone resorption-related inflammatory cytokines through an autocrine mechanism involving celecoxib-blocked PGs, mainly PGE(2), in osteoblasts.
巻・号 55(9)
ページ 679-88
公開日 2010-9-1
DOI 10.1016/j.archoralbio.2010.06.003
PII S0003-9969(10)00157-3
PMID 20630498
MeSH 3T3 Cells Animals Bone Remodeling / drug effects Bone Remodeling / physiology* Celecoxib Cycloheximide / pharmacology Cyclooxygenase 2 Inhibitors / pharmacology* Cytokines / biosynthesis* Dental Stress Analysis Dinoprostone / antagonists & inhibitors Dinoprostone / biosynthesis Dinoprostone / pharmacology* Enzyme-Linked Immunosorbent Assay Inflammation Mediators / metabolism Interleukin-17 / pharmacology Interleukin-17 / physiology* Interleukins / biosynthesis Mice Osteoblasts / metabolism* Polymerase Chain Reaction Prostaglandin-Endoperoxide Synthases / biosynthesis* Protein Synthesis Inhibitors / pharmacology Pyrazoles / pharmacology RNA, Messenger / analysis Sulfonamides / pharmacology
IF 1.931
引用数 12
WOS 分野 DENTISTRY, ORAL SURGERY & MEDICINE
リソース情報
ヒト・動物細胞 MC3T3-E1(RCB1126)