Cytokine gene expression - part of host defence in pulpitis

被引:79
作者
Zehnder, M
Delaleu, N
Du, YL
Bickel, M
机构
[1] Columbia Univ, Sch Dent & Oral Surg, Div Endodont, New York, NY USA
[2] Univ Zurich, Clin Geriatr & Special Care Dent, CH-8028 Zurich, Switzerland
[3] Columbia Univ, Sch Publ Hlth, Dept Biostat, New York, NY USA
关键词
cytokine; pulp tissue; real-time PCR;
D O I
10.1016/S1043-4666(03)00116-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Analyses of cytokines mediating inflammatory reactions are key to understanding the etiopathology of various diseases. This study investigated differences in cytokine gene expression between pulps from healthy virgin teeth and from symptomatic vital teeth with severe caries lesions in a group of young, healthy individuals. The mRNA levels of IL-10, IL-6, IL-8, and IL-18 were measured concomitantly by quantitative real-time RT-PCR. IL-1alpha and IL-1beta were not expressed at significantly higher levels ill symptomatic versus clinically healthy pulps, while the difference was significant for the other cytokines (log-rank test, P < 0.05). A concordance test for independence revealed significant correlation between IL-1alpha and IL-1beta, and between IL-6, IL-8, and IL-18 mRNA levels (P < 0.05). The cytokine-specific differences revealed a differential significance of gene expression in cytokine regulation. The hypothesis that increase of cytokine mRNA expression is part of host reaction in pulpitis was corroborated by our observation. (C) 2003 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:84 / 88
页数:5
相关论文
共 22 条
[1]   A newly defined interleukin-1? [J].
Bazan, JF ;
Timans, JC ;
Kastelein, RA .
NATURE, 1996, 379 (6566) :591-591
[2]   Cloning of a novel receptor subunit, AcPL, required for interleukin-18 signaling [J].
Born, TL ;
Thomassen, E ;
Bird, TA ;
Sims, JE .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (45) :29445-29450
[3]  
Cullinan EB, 1998, J IMMUNOL, V161, P5614
[4]   IL-18:: A TH1-inducing, proinflammatory cytokine and new member of the IL-1 family [J].
Dinarello, CA .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1999, 103 (01) :11-24
[5]   Biologic basis for interleukin-1 in disease [J].
Dinarello, CA .
BLOOD, 1996, 87 (06) :2095-2147
[6]   Interleukin-1β, interleukin-18, and the interleukin-1β converting enzyme [J].
Dinarello, CA .
MOLECULAR MECHANISMS OF FEVER, 1998, 856 :1-11
[7]   Interleukin-18 and interleukin-1β:: Two cytokine substrates for ICE (Caspase-1) [J].
Fantuzzi, G ;
Dinarello, CA .
JOURNAL OF CLINICAL IMMUNOLOGY, 1999, 19 (01) :1-11
[8]  
Fantuzzi G, 1997, J IMMUNOL, V158, P1818
[9]   Induction of rapid IL-1 beta mRNA degradation in THP-1 cells mediated through the Au-rich region in the 3'UTR by a radicicol analogue [J].
Kastelic, T ;
Schnyder, J ;
Leutwiler, A ;
Traber, R ;
Streit, B ;
Niggli, H ;
MacKenzie, A ;
Cheneval, D .
CYTOKINE, 1996, 8 (10) :751-761
[10]  
KUNO K, 1993, J BIOL CHEM, V268, P13510