Cytokines in Sepsis: Potent Immunoregulators and Potential Therapeutic Targets-An Updated View

被引:553
作者
Schulte, Wibke [1 ,2 ]
Bernhagen, Juergen [2 ]
Bucala, Richard [1 ]
机构
[1] Yale Univ, Sch Med, Dept Internal Med, Anlyan Ctr, New Haven, CT 06520 USA
[2] Rhein Westfal TH Aachen, Univ Hosp, Inst Biochem & Mol Cell Biol, D-52074 Aachen, Germany
基金
美国国家卫生研究院;
关键词
MIGRATION-INHIBITORY-FACTOR; TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR-BETA; ACTIVATED PROTEIN-C; SYSTEMIC INFLAMMATORY RESPONSE; COLONY-STIMULATING FACTOR; BLOOD MONONUCLEAR-CELLS; INNATE IMMUNE-RESPONSES; COLI SEPTIC SHOCK; INTERFERON-GAMMA;
D O I
10.1155/2013/165974
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Sepsis and septic shock are among the leading causes of death in intensive care units worldwide. Numerous studies on their pathophysiology have revealed an imbalance in the inflammatory network leading to tissue damage, organ failure, and ultimately, death. Cytokines are important pleiotropic regulators of the immune response, which have a crucial role in the complex pathophysiology underlying sepsis. They have both pro- and anti-inflammatory functions and are capable of coordinating effective defense mechanisms against invading pathogens. On the other hand, cytokines may dysregulate the immune response and promote tissue-damaging inflammation. In this review, we address the current knowledge of the actions of pro- and anti-inflammatory cytokines in sepsis pathophysiology as well as how these cytokines and other important immunomodulating agents may be therapeutically targeted to improve the clinical outcome of sepsis.
引用
收藏
页数:16
相关论文
共 232 条
[1]  
Aikawa N, 1996, Nihon Geka Gakkai Zasshi, V97, P771
[2]   Pathogen recognition and innate immunity [J].
Akira, S ;
Uematsu, S ;
Takeuchi, O .
CELL, 2006, 124 (04) :783-801
[3]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[4]   ISO-1 binding to the tautomerase active site of MIF inhibits its pro-inflammatory activity and increases survival in severe sepsis [J].
Al-Abed, Y ;
Dabideen, D ;
Aljabari, B ;
Valster, A ;
Messmer, D ;
Ochani, M ;
Tanovic, M ;
Ochani, K ;
Bacher, M ;
Nicoletti, F ;
Metz, C ;
Pavlov, VA ;
Miller, EJ ;
Tracey, KJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (44) :36541-36544
[5]   Systemic inflammatory response and progression to severe sepsis in critically ill infected patients [J].
Alberti, C ;
Brun-Buisson, C ;
Chevret, S ;
Antonelli, M ;
Goodman, SV ;
Martin, C ;
Moreno, R ;
Ochagavia, AR ;
Palazzo, M ;
Werdan, K ;
Le Gall, JR .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2005, 171 (05) :461-468
[6]   Influence of systemic inflammatory response syndrome and sepsis on outcome of critically ill infected patients [J].
Alberti, C ;
Brun-Buisson, C ;
Goodman, SV ;
Guidici, D ;
Granton, J ;
Moreno, R ;
Smithies, M ;
Thomas, O ;
Artigas, A ;
Le Gall, JR .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2003, 168 (01) :77-84
[7]   Human endotoxemia and human sepsis: limits to the model [J].
Anel, R ;
Kumar, A .
CRITICAL CARE, 2005, 9 (02) :151-152
[8]   Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care [J].
Angus, DC ;
Linde-Zwirble, WT ;
Lidicker, J ;
Clermont, G ;
Carcillo, J ;
Pinsky, MR .
CRITICAL CARE MEDICINE, 2001, 29 (07) :1303-1310
[9]  
[Anonymous], 2008, INTENS CARE MED, DOI [DOI 10.1007/s00134-007-0934-2, DOI 10.1007/s00134-008-1040-9]
[10]   Abrogation of macrophage migration inhibitory factor decreases West Nile virus lethality by limiting viral neuroinvasion [J].
Arjona, Alvaro ;
Foellmer, Harald G. ;
Town, Terrence ;
Leng, Lin ;
McDonald, Courtney ;
Wang, Tian ;
Wong, Susan J. ;
Montgomery, Ruth R. ;
Fikrig, Erol ;
Bucala, Richard .
JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (10) :3059-3066