We investigated the effects of two anti-inflammatory cytokines, interleukin (IL)-4 and IL-10, on the production of two proinflammatory cytokines, tumor necrosis factor (TNF)-alpha and IL-6, induced by titanium-alloy (Ti6Al4V) particles. Human monocytes isolated from the peripheral blood of six healt
Silica–ceramic suppresses the expression of proinflammatory cytokines induced by lipopolysaccharide in macrophages
✍ Scribed by Meeyul Hwang; Kwan-Kyu Park; Young-Chae Chang; Young-Ae Choo; Jae-Pil Jeon; Im-Hee Shin; Tae-Sung Lee
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 273 KB
- Volume
- 80A
- Category
- Article
- ISSN
- 1549-3296
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✦ Synopsis
Abstract
Bioactive materials have previously been used to coat implants. In a new development for bioactive materials, a silica–ceramic mixture was found to alleviate pain (Lee, Poster presented at the Ninth World Congress of Gynecological Endocrinology, Hongkong, 2001. Poster session (p47)). Here, we hypothesized that silica–ceramic can reduce the expression and activity of cyclooxygenase 2 (COX2) or cytokines associated with inflammation. The production of COX2 and proinflammatory cytokines was investigated by reverse transcriptase (RT)‐PCR and ELISA assay in macrophages stimulated by lipopolysaccharide (LPS). Silica–ceramic had no effect of COX2 expression and prostaglandin production in macrophages. However, silica–ceramic suppressed the synthesis of cytokines involved in inflammation, in particular, the expression of IL‐1β and IL‐6 was reduced at the transcriptional and translational levels. The involvement of NF‐κB in the suppression of cytokines by silica–ceramic was examined by luciferase reporter assay. The NF‐κB activity stimulated by LPS was inhibited by 20–60% with silica–ceramic compared with treatment with LPS alone. We suggest that inhibition of NF‐κB activity by silica–ceramic might cause the attenuation of proinflammatory cytokine expression in macrophages. In conclusion, silica–ceramic could be an alternative approach to regulate the inflammation process. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
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