View : 19 Download: 0
Effects of IL-1 beta, TNF-alpha, and TGF-beta on ciliary beat frequency of human nasal ciliated epithelial cells in vitro
- Effects of IL-1 beta, TNF-alpha, and TGF-beta on ciliary beat frequency of human nasal ciliated epithelial cells in vitro
- Rhee, CS; Hong, SK; Min, YG; Lee, CH; Lee, KS; Ahn, SH; Park, KS; Yi, WJ
- Ewha Authors
- Issue Date
- Journal Title
- AMERICAN JOURNAL OF RHINOLOGY
- vol. 13, no. 1, pp. 27 - 30
- OCEAN SIDE PUBLICATIONS INC
- Previous reports suggested that several cytokines may influence the ciliary brat of the airway ciliated epithelial cells. The aim of this study is to determine the effects of cytokines including IL-1 beta, TNF-alpha, and TGF-beta on ciliary beat frequency (CBF) of human nasal ciliated epithelial cells. CBF of cultured human nasal ciliated epithelial cells was measured 24 hours after incubating with concentrations of 0.01 ng/mL, 0.1 ng/mL, I ng/mL, 10 ng/mL, and 100 ng/mL of each recombinant human (rh) cytokine including rhIL-1 beta, rhTNF-alpha, and rhTGF-beta. CBF,was measured with time at concentrations of I ng/mL of rhIL-1 beta, 10 ng/mL of TNF-alpha, and I ng/mL of TGF-beta solutions. CBF of the human nasal ciliated epithelial cells increased after addition of rhIL-1 beta and rhTNF-alpha. Maximum CBF was observed at 1 ng/mL, of rhIL-1 beta and at 10 ng/mL. of rhTNF-alpha. CBF increased progressively to 4 hours after addition of rhIL-1 beta and rhTNF-alpha. Increased CBF sustained for 24 hours and decreased by 2 days. However; no variation of CBF,was observed after addition of I hTGF-beta, regardless of concentrations and time. The results of this study suggest that during acute inflammation, IL-1 beta and TNF-alpha may have a potential role in defense mechanism of human nasal epithelium by regulating CBF of the nasal ciliated epithelial cells.
- Appears in Collections:
- 의학전문대학원 > 의학과 > Journal papers
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.