Intravascular leukocyte migration through platelet thrombi: directing leukocytes to sites of vascular injury

被引:51
作者
Ghasemzadeh, Mehran [1 ,2 ]
Hosseini, Ehteramolsadat [1 ,3 ]
机构
[1] Blood Transfus Res Ctr, High Inst Res & Educ Transfus Med, Iranian Blood Transfusion Org Bldg,POB 14665-115, Tehran, Iran
[2] Monash Univ, Australian Ctr Blood Dis, Melbourne, Vic 3004, Australia
[3] Monash Univ, Dept Immunol Alfred Med Res & Educ Precinc, Melbourne, Vic 3004, Australia
关键词
Platelet-leukocyte crosstalk; NETs formation; intravascular leukocyte migration; neutrophil induced atherosclerosis; NEUTROPHIL EXTRACELLULAR TRAPS; SURFACE-ADHERENT PLATELETS; VON-WILLEBRAND-FACTOR; TISSUE FACTOR; IN-VIVO; P-SELECTIN; ACTIVATING-FACTOR; INTEGRIN ALPHA(IIB)BETA(3); ARTERIAL THROMBOSIS; PRIMARY HEMOSTASIS;
D O I
10.1160/TH14-08-0662
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Leukocytes recruitment to thrombi supports an intimate cellular interaction leading to the enhancement of pro-coagulant functions and pro-inflammatory responses at site of vascular injury. Recent observations of neutrophil extracellular traps (NETs) formation and its mutual reactions with platelet thrombi adds more clinical interest to the growing body of knowledge in the field of platelet-leukocyte crosstalk. However, having considered thrombus as a barrier between leukocytes and injured endothelium, the full inflammatory roles of these cells during thrombosis is still ill defined. The most recent observation of neutrophils migration into the thrombi is a phenomenon that highlights the inflammatory functions of leukocytes at the site of injury. It has been hypothesised that leukocytes migration might be associated with the conveyance of highly reactive pro-inflammatory and/or pro-coagulant mediators to sites of vascular injury. In addition, the evidence of neutrophils migration into arterial thrombi following traumatic and ischaemia-reperfusion injury highlights the already described role of these cells in atherosclerosis. Regardless of the mechanisms behind leukocyte migration, whether these migrated cells benefit normal homeostasis by their involvement in wound healing and vascular rebuilding or they increase unwilling inflammatory responses, could be of interest for future researches that provide new insight into biological importance of leukocyte recruitment to thrombi.
引用
收藏
页码:1224 / 1235
页数:12
相关论文
共 145 条
[1]   Lipid raft adhesion receptors and Syk regulate selectin-dependent rolling under flow conditions [J].
Abbal, Claire ;
Lambelet, Martine ;
Bertaggia, Debora ;
Gerbex, Carole ;
Martinez, Manuel ;
Arcaro, Alexandre ;
Schapira, Marc ;
Spertini, Olivier .
BLOOD, 2006, 108 (10) :3352-3359
[2]   Neutrophil Function: From Mechanisms to Disease [J].
Amulic, Borko ;
Cazalet, Christel ;
Hayes, Garret L. ;
Metzler, Kathleen D. ;
Zychlinsky, Arturo .
ANNUAL REVIEW OF IMMUNOLOGY, VOL 30, 2012, 30 :459-489
[3]   Neutrophil extracellular traps (NETs) and the role of platelets in infection [J].
Andrews, Robert K. ;
Arthur, Jane F. ;
Gardiner, Elizabeth E. .
THROMBOSIS AND HAEMOSTASIS, 2014, 112 (04) :659-665
[4]   Laser-induced endothelial cell activation supports fibrin formation [J].
Atkinson, Ben T. ;
Jasuja, Reema ;
Chen, Vivien M. ;
Nandivada, Prathima ;
Furie, Bruce ;
Furie, Barbara C. .
BLOOD, 2010, 116 (22) :4675-4683
[5]   Platelets adhered to endothelial cell-bound ultra-large von Willebrand factor strings support leukocyte tethering and rolling under high shear stress [J].
Bernardo, A ;
Ball, C ;
Nolasco, L ;
Choi, H ;
Moake, JL ;
Dong, JF .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2005, 3 (03) :562-570
[6]   Primary haemostasis: newer insights [J].
Berndt, M. C. ;
Metharom, P. ;
Andrews, R. K. .
HAEMOPHILIA, 2014, 20 :15-22
[7]   Integrin signalling in neutrophils and macrophages [J].
Berton, G ;
Lowell, CA .
CELLULAR SIGNALLING, 1999, 11 (09) :621-635
[8]   ENDOTHELIAL LEUKOCYTE ADHESION MOLECULE-1 - AN INDUCIBLE RECEPTOR FOR NEUTROPHILS RELATED TO COMPLEMENT REGULATORY PROTEINS AND LECTINS [J].
BEVILACQUA, MP ;
STENGELIN, S ;
GIMBRONE, MA ;
SEED, B .
SCIENCE, 1989, 243 (4895) :1160-1165
[9]   Molecular and cellular mechanisms of myocardial stunning [J].
Bolli, R ;
Marbán, E .
PHYSIOLOGICAL REVIEWS, 1999, 79 (02) :609-634
[10]   NEUTROPHILS CAN GENERATE THEIR ACTIVATOR NEUTROPHIL-ACTIVATING PEPTIDE-2 BY PROTEOLYTIC CLEAVAGE OF PLATELET-DERIVED CONNECTIVE TISSUE-ACTIVATING PEPTIDE-III [J].
BRANDT, E ;
VANDAMME, J ;
FLAD, HD .
CYTOKINE, 1991, 3 (04) :311-321