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本文引用的文献

1
The complement anaphylatoxin C5a induces apoptosis in adrenomedullary cells during experimental sepsis.在实验性脓毒症期间,补体过敏毒素C5a可诱导肾上腺髓质细胞凋亡。
PLoS One. 2008 Jul 2;3(7):e2560. doi: 10.1371/journal.pone.0002560.
2
Functions of the complement components C3 and C5 during sepsis.补体成分C3和C5在脓毒症中的作用。
FASEB J. 2008 Oct;22(10):3483-90. doi: 10.1096/fj.08-110595. Epub 2008 Jun 27.
3
Functional roles for C5a receptors in sepsis.C5a受体在脓毒症中的功能作用
Nat Med. 2008 May;14(5):551-7. doi: 10.1038/nm1753. Epub 2008 May 4.
4
HMGB1: endogenous danger signaling.高迁移率族蛋白B1:内源性危险信号
Mol Med. 2008 Jul-Aug;14(7-8):476-84. doi: 10.2119/2008-00034.Klune.
5
Dendritic cell PAR1-S1P3 signalling couples coagulation and inflammation.树突状细胞的PAR1-S1P3信号传导将凝血与炎症联系起来。
Nature. 2008 Apr 3;452(7187):654-8. doi: 10.1038/nature06663. Epub 2008 Feb 27.
6
Adverse functions of IL-17A in experimental sepsis.白细胞介素-17A在实验性脓毒症中的不良作用。
FASEB J. 2008 Jul;22(7):2198-205. doi: 10.1096/fj.07-105221. Epub 2008 Feb 25.
7
HMGB1 develops enhanced proinflammatory activity by binding to cytokines.高迁移率族蛋白B1(HMGB1)通过与细胞因子结合而产生增强的促炎活性。
J Immunol. 2008 Feb 15;180(4):2531-7. doi: 10.4049/jimmunol.180.4.2531.
8
Host-pathogen interactions in sepsis.脓毒症中的宿主-病原体相互作用
Lancet Infect Dis. 2008 Jan;8(1):32-43. doi: 10.1016/S1473-3099(07)70265-7. Epub 2007 Dec 11.
9
'Role reversal' for the receptor PAR1 in sepsis-induced vascular damage.脓毒症诱导的血管损伤中受体PAR1的“角色反转”
Nat Immunol. 2007 Dec;8(12):1303-12. doi: 10.1038/ni1525. Epub 2007 Oct 28.
10
TLR4/MD-2 monoclonal antibody therapy affords protection in experimental models of septic shock.TLR4/MD-2单克隆抗体疗法在脓毒性休克实验模型中具有保护作用。
J Immunol. 2007 Nov 1;179(9):6107-14. doi: 10.4049/jimmunol.179.9.6107.

脓毒症中的有害分子机制。

Harmful molecular mechanisms in sepsis.

作者信息

Rittirsch Daniel, Flierl Michael A, Ward Peter A

机构信息

Department of Pathology, The University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, Michigan 48109-0602, USA.

出版信息

Nat Rev Immunol. 2008 Oct;8(10):776-87. doi: 10.1038/nri2402.

DOI:10.1038/nri2402
PMID:18802444
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2786961/
Abstract

Sepsis and sepsis-associated multi-organ failure are major challenges for scientists and clinicians and are a tremendous burden for health-care systems. Despite extensive basic research and clinical studies, the pathophysiology of sepsis is still poorly understood. We are now beginning to understand that sepsis is a heterogeneous, dynamic syndrome caused by imbalances in the 'inflammatory network'. In this Review, we highlight recent insights into the molecular interactions that occur during sepsis and attempt to unravel the nature of the dysregulated immune response during sepsis.

摘要

脓毒症及脓毒症相关的多器官功能衰竭是科学家和临床医生面临的重大挑战,也是卫生保健系统的巨大负担。尽管进行了广泛的基础研究和临床研究,但脓毒症的病理生理学仍未得到充分理解。我们现在开始认识到,脓毒症是一种由“炎症网络”失衡引起的异质性、动态综合征。在本综述中,我们重点介绍了对脓毒症期间发生的分子相互作用的最新见解,并试图阐明脓毒症期间免疫反应失调的本质。