Aspects on pathophysiological mechanisms in COPD

被引:73
作者
Larsson, Kjell [1 ]
机构
[1] Karolinska Inst, Natl Inst Environm Med, Unit Lung & Allergy Res, SE-17177 Stockholm, Sweden
关键词
chemokines; COPD; cytokines; emphysema inflammation; review;
D O I
10.1111/j.1365-2796.2007.01837.x
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
Larsson K (Karolinska Institutet, Stockholm, Sweden). Aspects on pathophysiological mechanisms in COPD (Review). J Intern Med 2007; 262: 311-340. Chronic obstructive pulmonary disease (COPD) is a condition which is characterized by irreversible airway obstruction due to narrowing of small airways, bronchiolitis, and destruction of the lung parenchyma, emphysema. It is the fourth most common cause of mortality in the world and is expected to be the third most common cause of death by 2020. The main cause of COPD is smoking but other exposures may be of importance. Exposure leads to airway inflammation in which a variety of cells are involved. Besides neutrophil granulocytes, macrophages and lymphocytes, air -way epithelial cells are also of particular importance in the inflammatory process and in the development of emphysema. Cell trafficking orchestrated by chemokines and other chamoattractants, the proteinase-antiproteinase system, oxidative stress and airway remodelling are central processes associated with the development of COPD. Recently systemic effects of COPD have attracted attention and the importance of systemic inflammation has been recognized. This seems to have direct therapeutic implications as treatment with inhaled glucocorticosteroids has been shown to influence mortality. The increasing body of knowledge regarding the inflammatory mechanism in COPD will most likely have implications for future therapy and new drugs, specifically aimed at interaction with the inflammatory processes, are currently being developed.
引用
收藏
页码:311 / 340
页数:30
相关论文
共 335 条
[1]
Neutrophil defensins enhance lung epithelial wound closure and mucin gene expression in vitro [J].
Aarbiou, J ;
Verhoosel, RM ;
van Wetering, S ;
de Boer, WI ;
van Krieken, JHJM ;
Litvinov, SV ;
Rabe, KF ;
Hiemstra, PS .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2004, 30 (02) :193-201
[2]
Aarvak T, 1999, J IMMUNOL, V162, P1246
[3]
ABBOUD RT, 1985, AM REV RESPIR DIS, V131, P79
[4]
ENDOTHELIAL AND EPITHELIAL-CELL ADHESION MOLECULES [J].
ALBELDA, SM .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1991, 4 (03) :195-203
[5]
Circulating monocytes from healthy individuals and COPD patients [J].
Aldonyte, R ;
Jansson, L ;
Piitulainen, E ;
Janciauskiene, S .
RESPIRATORY RESEARCH, 2003, 4 (11)
[6]
ALESSANDRI C, 1994, THROMB HAEMOSTASIS, V72, P343
[7]
PROGNOSIS IN CHRONIC OBSTRUCTIVE PULMONARY-DISEASE [J].
ANTHONISEN, NR ;
WRIGHT, EC ;
HODGKIN, JE ;
HOPEWELL, PC ;
LEVIN, DC ;
STEVENS, PM .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1986, 133 (01) :14-20
[8]
Epidemiology of chronic obstructive pulmonary disease [J].
Antó, JM ;
Vermeire, P ;
Vestbo, J ;
Sunyer, J .
EUROPEAN RESPIRATORY JOURNAL, 2001, 17 (05) :982-994
[9]
Aoshiba K, 2001, AM J PHYSIOL-LUNG C, V281, pL556
[10]
IL-13-induced changes in the goblet cell density of human bronchial epithelial cell cultures: MAP kinase and phosphatidylinositol 3-kinase regulation [J].
Atherton, HC ;
Jones, G ;
Danahay, H .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2003, 285 (03) :L730-L739