Platelets, endothelium and shear join forces to mislead neutrophils in sepsis

被引:5
作者
Paula Neto, Heitor A. [1 ]
Kubes, Paul [1 ]
机构
[1] Univ Calgary, Immunol Res Grp, Dept Physiol & Pharmacol, Calvin Phoebe & Joan Snyder Inst Infect Immun & I, Calgary, AB T2N 4N1, Canada
来源
CRITICAL CARE | 2011年 / 15卷 / 01期
关键词
ACTIVATION;
D O I
10.1186/cc9371
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Neutrophils are circulating leukocytes with great cytotoxic potential, responsible for the first combat against invading pathogens. Their accumulation in tissues must be highly controlled so that the number of neutrophils delivered to the affected site is sufficient to control infection with minimum injury to the surrounding healthy tissue. In sepsis, neutrophil migration is dysregulated - resulting in insufficient delivery of neutrophils to the infectious site and massive neutrophil accumulation in uninfected organs. This dysregulation has the potential to cause inappropriate tissue injury that may explain the multiple organ dysfunction observed in severe sepsis. A better understanding of the mechanisms that contribute to this process is fundamental to design therapeutic strategies to circumvent tissue injury and organ dysfunction in sepsis.
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页数:2
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共 12 条
[1]   NEUTROPHIL PARALYSIS IN SEPSIS [J].
Alves-Filho, Jose C. ;
Spiller, Fernando ;
Cunha, Fernando Q. .
SHOCK, 2010, 34 :15-21
[2]   Platelets express functional Toll-like receptor-4 [J].
Andonegui, G ;
Kerfoot, SM ;
McNagny, K ;
Ebbert, KVJ ;
Patel, KD ;
Kubes, P .
BLOOD, 2005, 106 (07) :2417-2423
[3]   Neutrophils, from Marrow to Microbes [J].
Borregaard, Niels .
IMMUNITY, 2010, 33 (05) :657-670
[4]   Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood [J].
Clark, Stephen R. ;
Ma, Adrienne C. ;
Tavener, Samantha A. ;
McDonald, Braedon ;
Goodarzi, Zahra ;
Kelly, Margaret M. ;
Patel, Kamala D. ;
Chakrabarti, Subhadeep ;
McAvoy, Erin ;
Sinclair, Gary D. ;
Keys, Elizabeth M. ;
Allen-Vercoe, Emma ;
DeVinney, Rebekah ;
Doig, Christopher J. ;
Green, Francis H. Y. ;
Kubes, Paul .
NATURE MEDICINE, 2007, 13 (04) :463-469
[5]   Chemokines, chemokine receptors and adhesion molecules on different human endothelia: discriminating the tissue-specific functions that affect leucocyte migration [J].
Hillyer, P ;
Mordelet, E ;
Flynn, G ;
Male, D .
CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2003, 134 (03) :431-441
[6]   Leukocyte activation in sepsis; correlations with disease state and mortality [J].
Kobold, ACM ;
Tulleken, JE ;
Zijlstra, JG ;
Sluiter, W ;
Hermans, J ;
Kallenberg, CGM ;
Tervaert, JWC .
INTENSIVE CARE MEDICINE, 2000, 26 (07) :883-892
[7]   Interaction of CD44 and hyaluronan is the dominant mechanism for neutrophil sequestration in inflamed liver sinusoids [J].
McDonald, Braedon ;
McAvoy, Erin F. ;
Lam, Florence ;
Gill, Varinder ;
de la Motte, Carol ;
Savani, Rashmin C. ;
Kubes, Paul .
JOURNAL OF EXPERIMENTAL MEDICINE, 2008, 205 (04) :915-927
[8]   Selective Down-Regulation of Neutrophil Mac-1 in Endotoxemic Hepatic Microcirculation via IL-10 [J].
Menezes, Gustavo Batista ;
Lee, Woo-Yong ;
Zhou, Hong ;
Waterhouse, Christopher Curtis Matchett ;
Cara, Denise Carmona ;
Kubes, Paul .
JOURNAL OF IMMUNOLOGY, 2009, 183 (11) :7557-7568
[9]   The physiology of leukocyte recruitment: An in vivo perspective [J].
Petri, Bjoern ;
Phillipson, Mia ;
Kubes, Paul .
JOURNAL OF IMMUNOLOGY, 2008, 180 (10) :6439-6446
[10]   Mechanisms of leukocyte distribution during sepsis: an experimental study on the interdependence of cell activation, shear stress and endothelial injury [J].
Ploppa, Annette ;
Schmidt, Volker ;
Hientz, Andreas ;
Reutershan, Joerg ;
Haeberle, Helene A. ;
Nohe, Boris .
CRITICAL CARE, 2010, 14 (06)