Chemokines in acute respiratory distress syndrome

被引:261
作者
Puneet, P
Moochhala, S
Bhatia, M
机构
[1] Natl Univ Singapore, Fac Med, Dept Pharmacol, Singapore 117597, Singapore
[2] Def Med & Environm Res Inst, Ctr Biomed Sci, Singapore, Singapore
关键词
inflammatory mediators; polymorphonuclear leukocyte; pathogenesis; antagonists;
D O I
10.1152/ajplung.00405.2003
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
A characteristic feature of all inflammatory disorders is the excessive recruitment of leukocytes to the site of inflammation. The loss of control in trafficking these cells contributes to inflammatory diseases. Leukocyte recruitment is a well-orchestrated process that includes several protein families including the large cytokine subfamily of chemotactic cytokines, the chemokines. Chemokines and their receptors are involved in the pathogenesis of several diseases. Acute lung injury that clinically manifests as acute respiratory distress syndrome ( ARDS) is caused by an uncontrolled systemic inflammatory response resulting from clinical events including major surgery, trauma, multiple transfusions, severe burns, pancreatitis, and sepsis. Systemic inflammatory response syndrome involves activation of alveolar macrophages and sequestered neutrophils in the lung. The clinical hallmarks of ARDS are severe hypoxemia, diffuse bilateral pulmonary infiltrates, and normal intracardiac filling pressures. The magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ARDS. Recent evidence shows that activated leukocytes and chemokines play a key role in the pathogenesis of ARDS. The expanding number of antagonists of chemokine receptors for inflammatory disorders may hold promise for new medicines to combat ARDS.
引用
收藏
页码:L3 / L15
页数:13
相关论文
共 122 条
[91]   FLUID BALANCE DURING PULMONARY-EDEMA - IS FLUID GAIN A MARKER OR A CAUSE OF POOR OUTCOME [J].
SCHULLER, D ;
MITCHELL, JP ;
CALANDRINO, FS ;
SCHUSTER, DP .
CHEST, 1991, 100 (04) :1068-1075
[92]   Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema [J].
Schutte, H ;
Lohmeyer, J ;
Rosseau, S ;
Ziegler, S ;
Siebert, C ;
Kielisch, H ;
Pralle, H ;
Grimminger, F ;
Morr, H ;
Seeger, W .
EUROPEAN RESPIRATORY JOURNAL, 1996, 9 (09) :1858-1867
[93]   Recent developments in modulating chemokine networks [J].
Schwarz, MK ;
Wells, TNC .
EXPERT OPINION ON THERAPEUTIC PATENTS, 1999, 9 (11) :1471-1490
[94]   Immunology - Mobilizing the army [J].
Shapiro, SD .
NATURE, 2003, 421 (6920) :223-224
[95]   Levels of the chemokines growth-related oncogene α and epithelial neutrophil-activating protein 78 are raised in patients with severe acute pancreatitis [J].
Shokuhi, S ;
Bhatia, M ;
Christmas, S ;
Sutton, R ;
Neoptolemos, JP ;
Slavin, J .
BRITISH JOURNAL OF SURGERY, 2002, 89 (05) :566-572
[96]  
SOZZANI S, 1994, J IMMUNOL, V152, P3615
[97]  
STANDIFORD TJ, 1991, J BIOL CHEM, V266, P9912
[98]   EVOLUTION OF BRONCHOALVEOLAR CELL-POPULATIONS IN THE ADULT-RESPIRATORY-DISTRESS-SYNDROME [J].
STEINBERG, KP ;
MILBERG, JA ;
MARTIN, TR ;
MAUNDER, RJ ;
COCKRILL, BA ;
HUDSON, LD .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1994, 150 (01) :113-122
[99]   Chemokines in lung injury - Thomas A. Neff lecture [J].
Strieter, RM ;
Kunkel, SL ;
Keane, MP ;
Standiford, TJ .
CHEST, 1999, 116 (01) :103S-110S
[100]   CYTOKINES .2. CYTOKINES AND LUNG INFLAMMATION - MECHANISMS OF NEUTROPHIL RECRUITMENT TO THE LUNG [J].
STRIETER, RM ;
LUKACS, NW ;
STANDIFORD, TJ ;
KUNKEL, SL .
THORAX, 1993, 48 (07) :765-769