Increased expression of nuclear factor-κB in bronchial biopsies from smokers and patients with COPD

被引:314
作者
Di Stefano, A
Caramori, G
Oates, T
Capelli, A
Lusuardi, M
Gnemmi, I
Ioli, F
Chung, KF
Donner, CF
Barnes, PJ
Adcock, IM
机构
[1] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, Dept Thorac Med, Sch Med, London SW3 6LY, England
[2] IRCCS, Salvatore Maugeri Fdn, Med Ctr Rehabil, Div Pulm Dis, Veruno, Italy
关键词
airflow limitation; airway inflammation; nuclear factor-kappa B; T-lymphocytes;
D O I
10.1183/09031936.02.00272002
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
The expression of nuclear factor (NF)-kappaB is an indicator of cellular activation and of inflammatory mediator production. The aim of the present study was to characterise the expression and localisation of p65, the major subunit Of NF-kappaB, in the bronchial mucosa of patients with chronic obstructive pulmonary disease (COPD), and to examine the relationship between p65 expression and disease status. Bronchial biopsies were obtained from 14 smokers with COPD, 17 smokers with normal lung function and 12 nonsmokers with normal lung function. The number of p65 positive (+) cells was quantified by immunohistochemistry and the expression of p65 in bronchial biopsies from the three groups was examined by Western blotting (WB). Smokers with normal lung function and patients with COPD had increased numbers of p65+ cells in the epithelium and increased p65 nuclear expression. In COPD patients the number of epithelial p65+ cells correlated with the degree of airflow limitation. WB analysis showed an increase in p65 in smokers with normal lung function and COPI) patients (p<0.05). Bronchial biopsies in smokers with normal lung function and chronic obstructive pulmonary disease patients show increased expression of p65 protein, predominantly in the bronchial epithelium, Disease severity is associated with an increased epithelial expression of nuclear factor-kappaB.
引用
收藏
页码:556 / 563
页数:8
相关论文
共 32 条
[1]
The transcription factor NF-κB and human disease [J].
Baldwin, AS .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (01) :3-6
[3]
New therapies for chronic obstructive pulmonary disease [J].
Barnes, PJ .
THORAX, 1998, 53 (02) :137-147
[4]
Mechanisms of disease - Nuclear factor-kappa b - A pivotal transcription factor in chronic inflammatory diseases [J].
Barnes, PJ ;
Larin, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (15) :1066-1071
[5]
Increased MCP-1 and MIP-1β in bronchoalveolar lavage fluid of chronic bronchitics [J].
Capelli, A ;
Di Stefano, A ;
Gnemmi, I ;
Balbo, P ;
Cerutti, CG ;
Balbi, B ;
Lusuardi, M ;
Donner, CF .
EUROPEAN RESPIRATORY JOURNAL, 1999, 14 (01) :160-165
[6]
Expression of GATA family of transcription factors in T-cells, monocytes and bronchial biopsies [J].
Caramori, G ;
Lim, S ;
Ito, K ;
Tomita, K ;
Oates, T ;
Jazrawi, E ;
Chung, KF ;
Barnes, PJ ;
Adcock, IM .
EUROPEAN RESPIRATORY JOURNAL, 2001, 18 (03) :466-473
[7]
Interleukin 8 in bronchoalveolar lavage of asthmatic and chronic bronchitis patients [J].
Chanez, P ;
Enander, I ;
Jones, I ;
Godard, P ;
Bousquet, J .
INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 1996, 111 (01) :83-88
[8]
The role of nuclear factor-κ B in pulmonary diseases [J].
Christman, JW ;
Sadikot, RT ;
Blackwell, TS .
CHEST, 2000, 117 (05) :1482-1487
[9]
Communaute Europeenne du Charbon et de l'Acier (CECA), 1971, TABL REF EX SPIR
[10]
*COPD GUID GROUP S, 1997, THORAX S5, V52, pS1