Procoagulant alveolar microparticles in the lungs of patients with acute respiratory distress syndrome

被引:127
作者
Bastarache, Julie A. [1 ]
Fremont, Richard D. [1 ]
Kropski, Jonathan A. [1 ]
Bossert, Frederick R. [1 ]
Ware, Lorraine B. [1 ]
机构
[1] Vanderbilt Univ, Sch Med, Div Allergy Pulm & Crit Care Med, Nashville, TN 37232 USA
基金
美国国家卫生研究院;
关键词
fibrin deposition; tissue factor; receptor for advanced glycation end products; hydrostatic pulmonary edema; CELL-DERIVED MICROPARTICLES; TISSUE-FACTOR; IN-VIVO; COAGULATION; INJURY; EXPRESSION; EPITHELIUM; RESOLUTION; MOLECULES; PLATELETS;
D O I
10.1152/ajplung.00214.2009
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Bastarache JA, Fremont RD, Kropski JA, Bossert FR, Ware LB. Procoagulant alveolar microparticles in the lungs of patients with acute respiratory distress syndrome. Am J Physiol Lung Cell Mol Physiol 297: L1035-L1041, 2009. First published August 21, 2009; doi:10.1152/ajplung.00214.2009.-Coagulation and fibrinolysis abnormalities are observed in acute lung injury (ALI) in both human disease and animal models and may contribute to ongoing inflammation in the lung. Tissue factor (TF), the main initiator of the coagulation cascade, is upregulated in the lungs of patients with ALI/acute respiratory distress syndrome (ARDS) and likely contributes to fibrin deposition in the air space. The mechanisms that govern TF upregulation and activation in the lung are not well understood. In the vascular space, TF-bearing microparticles (MPs) are central to clot formation and propagation. We hypothesized that TF-bearing MPs in the lungs of patients with ARDS contribute to the procoagulant phenotype in the air space during acute injury and that the alveolar epithelium is one potential source of TF MPs. We studied pulmonary edema fluid collected from patients with ARDS compared with a control group of patients with hydrostatic pulmonary edema. Patients with ARDS have higher concentrations of MPs in the lung compared with patients with hydrostatic edema (25.5 IQR 21.3-46.9 vs. 7.8 IQR 2.3-27.5 mu mol/l, P = 0.009 by Mann-Whitney U-test). These MPs are enriched for TF, have procoagulant activity, and likely originate from the alveolar epithelium [as measured by elevated levels of RAGE (receptor for advanced glycation end products) in ARDS MPs compared with hydrostatic MPs]. Furthermore, alveolar epithelial cells in culture release procoagulant TF MPs in response to a proinflammatory stimulus. These findings suggest that alveolar epithelial-derived MPs are one potential source of TF procoagulant activity in the air space in ARDS and that epithelial MP formation and release may represent a unique therapeutic target in ARDS.
引用
收藏
页码:L1035 / L1041
页数:7
相关论文
共 26 条
[1]   Induction of microparticle- and cell-associated intravascular tissue factor in human endotoxemia [J].
Aras, O ;
Shet, A ;
Bach, RR ;
Hysjulien, JL ;
Slungaard, A ;
Hebbel, RP ;
Escolar, G ;
Jilma, B ;
Key, NS .
BLOOD, 2004, 103 (12) :4545-4553
[2]   The significance of shed membrane particles during programmed cell death in vitro, and in vivo, in HIV-1 infection [J].
Aupeix, K ;
Hugel, B ;
Martin, T ;
Bischoff, P ;
Lill, H ;
Pasquali, JL ;
Freyssinet, JM .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (07) :1546-1554
[3]   The alveolar epithelium can initiate the extrinsic coagulation cascade through expression of tissue factor [J].
Bastarache, Julie A. ;
Wang, Ling ;
Geiser, Thomas ;
Wang, Zhengming ;
Albertine, Kurt H. ;
Matthay, Michael A. ;
Ware, Lorraine B. .
THORAX, 2007, 62 (07) :608-616
[4]  
Berckmans RJ, 2001, THROMB HAEMOSTASIS, V85, P639
[5]   Human cell-derived microparticles promote thrombus formation in vivo in a tissue factor-dependent manner [J].
Biró, É ;
Sturk-Maquelin, KN ;
Vogel, GMT ;
Meuleman, DG ;
Smit, MJ ;
Hack, CE ;
Sturk, A ;
Nieuwland, R .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2003, 1 (12) :2561-2568
[6]   AMERICAN-COLLEGE OF CHEST PHYSICIANS SOCIETY OF CRITICAL CARE MEDICINE CONSENSUS CONFERENCE - DEFINITIONS FOR SEPSIS AND ORGAN FAILURE AND GUIDELINES FOR THE USE OF INNOVATIVE THERAPIES IN SEPSIS [J].
BONE, RC ;
BALK, RA ;
CERRA, FB ;
DELLINGER, RP ;
FEIN, AM ;
KNAUS, WA ;
SCHEIN, RMH ;
SIBBALD, WJ ;
ABRAMS, JH ;
BERNARD, GR ;
BIONDI, JW ;
CALVIN, JE ;
DEMLING, R ;
FAHEY, PJ ;
FISHER, CJ ;
FRANKLIN, C ;
GORELICK, KJ ;
KELLEY, MA ;
MAKI, DG ;
MARSHALL, JC ;
MERRILL, WW ;
PRIBBLE, JP ;
RACKOW, EC ;
RODELL, TC ;
SHEAGREN, JN ;
SILVER, M ;
SPRUNG, CL ;
STRAUBE, RC ;
TOBIN, MJ ;
TRENHOLME, GM ;
WAGNER, DP ;
WEBB, CD ;
WHERRY, JC ;
WIEDEMANN, HP ;
WORTEL, CH .
CRITICAL CARE MEDICINE, 1992, 20 (06) :864-874
[7]   Mechanical ventilation with lower tidal volumes and positive end-expiratory pressure prevents alveolar coagulation in patients without lung injury [J].
Choi, Goda ;
Wolthuis, Esther K. ;
Bresser, Paul ;
Levi, Marcel ;
van der Poll, Tom ;
Dzoljic, Misa ;
Vroom, Margreeth B. ;
Schultz, Marcus J. .
ANESTHESIOLOGY, 2006, 105 (04) :689-695
[8]   Tissue-factor-bearing microvesicles arise from lipid rafts and fuse with activated platelets to initiate coagulation [J].
del Conde, I ;
Shrimpton, CN ;
Thiagarajan, P ;
López, JA .
BLOOD, 2005, 106 (05) :1604-1611
[9]  
Hussein MNA, 2003, J THROMB HAEMOST, V1, P2434
[10]   PROCOAGULANT ACTIVITY IN BRONCHOALVEOLAR LAVAGE IN THE ADULT RESPIRATORY-DISTRESS SYNDROME - CONTRIBUTION OF TISSUE FACTOR ASSOCIATED WITH FACTOR-VII [J].
IDELL, S ;
GONZALEZ, K ;
BRADFORD, H ;
MACARTHUR, CK ;
FEIN, AM ;
MAUNDER, RJ ;
GARCIA, JGN ;
GRIFFITH, DE ;
WEILAND, J ;
MARTIN, TR ;
MCLARTY, J ;
FAIR, DS ;
WALSH, PN ;
COLMAN, RW .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1987, 136 (06) :1466-1474