Effects of IL-1β, TNF-α, and TGF-β on ciliary beat frequency of human nasal ciliated epithelial cells in vitro

被引:17
作者
Rhee, CS
Hong, SK
Min, YG
Lee, CH
Lee, KS
Ahn, SH
Park, KS
Yi, WJ
机构
[1] Seoul Natl Univ, Coll Med, Dept Otorhinolaryngol, Chongno Gu, Seoul 110744, South Korea
[2] Seoul Natl Univ, Coll Med, Dept Biomed Engn, Chongno Gu, Seoul 110744, South Korea
[3] Ewha Womans Univ, Coll Med, Dept Otolaryngol, Seoul, South Korea
来源
AMERICAN JOURNAL OF RHINOLOGY | 1999年 / 13卷 / 01期
关键词
D O I
10.2500/105065899781389920
中图分类号
R76 [耳鼻咽喉科学];
学科分类号
100213 ;
摘要
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.
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页码:27 / 30
页数:4
相关论文
共 19 条
[1]  
ABBAS AK, 1994, CELLULAR MOL IMMUNOL, P245
[2]  
CROMWELL O, 1992, IMMUNOLOGY, V77, P330
[3]   QUANTITATION AND IMMUNOCYTOLOGICAL IDENTIFICATION OF INTERLEUKIN-1 IN NASAL POLYPS FROM PATIENTS WITH CHRONIC SINUSITIS [J].
HAMAGUCHI, Y ;
SUZUMURA, H ;
ARIMA, S ;
SAKAKURA, Y .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 1994, 104 (02) :155-159
[4]   INDUCTION OF NITRIC-OXIDE SYNTHASE IN ASTHMA [J].
HAMID, Q ;
SPRINGALL, DR ;
RIVEROSMORENO, V ;
CHANEZ, P ;
HOWARTH, P ;
REDINGTON, A ;
BOUSQUET, J ;
GODARD, P ;
HOLGATE, S ;
POLAK, JM .
LANCET, 1993, 342 (8886-7) :1510-1513
[5]  
Hattori Masahiko, 1994, Auris Nasus Larynx, V21, P219
[6]   RETENTION FLUIDS OF CHRONIC SINUSITIS INDUCE NEUTROPHIL ADHERENCE TO MICROVASCULAR ENDOTHELIAL-CELLS [J].
ITOH, K ;
KATAHIRA, S ;
MATSUZAKI, T ;
OHYAMA, M ;
FUKUDA, K .
ACTA OTO-LARYNGOLOGICA, 1992, 112 (05) :882-889
[7]   MODULATION OF AIRWAY EPITHELIAL-CELL CILIARY BEAT FREQUENCY BY NITRIC-OXIDE [J].
JAIN, B ;
RUBINSTEIN, I ;
ROBBINS, RA ;
LEISE, KL ;
SISSON, JH .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1993, 191 (01) :83-88
[8]  
JAIN B, 1995, AM J PHYSIOL, V268, P911
[9]   NITRIC-OXIDE SYNTHASE IN HUMAN AND RAT LUNG - IMMUNOCYTOCHEMICAL AND HISTOCHEMICAL-LOCALIZATION [J].
KOBZIK, L ;
BREDT, DS ;
LOWENSTEIN, CJ ;
DRAZEN, J ;
GASTON, B ;
SUGARBAKER, D ;
STAMLER, JS .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1993, 9 (04) :371-377
[10]  
LE JM, 1987, LAB INVEST, V56, P234