Chronic inflammation: a failure of resolution?

被引:252
作者
Lawrence, Toby [1 ]
Gilroy, Derek W.
机构
[1] Univ London Imperial Coll Sci Technol & Med, Fac Med, Kennedy Inst Rheumatol Div, London W6 8LH, England
[2] UCL, Dept Med, London W1N 8AA, England
关键词
acute inflammationn; chronic inflammation; eccosanoids; macrophage; resolution; signalling;
D O I
10.1111/j.1365-2613.2006.00507.x
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Inflammation has evolved as a protective response to insult or injury, it's a primordial response that eliminates or neutralises foreign organisms or material, the resolution of inflammation encompasses the endogenous anti-inflammatory mechanisms that protect us against excessive tissue injury and promote the restoration of tissue structure and function. In fact, our well being and survival depends upon its efficiency and carefully-balanced control. In general, the innate inflammatory response initiates within minutes and, if all is well, resolves within hours. In contrast, chronic inflammation persists for weeks, months or even years. Here, we are going to discuss the key endogenous checkpoints necessary for mounting an effective yet limited inflammatory response and the crucial biochemical pathways necessary to prevent its persistence.
引用
收藏
页码:85 / 94
页数:10
相关论文
共 64 条
[1]   The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immuneresponse [J].
Alexander, WS ;
Hilton, DJ .
ANNUAL REVIEW OF IMMUNOLOGY, 2004, 22 :503-529
[2]   Tumor necrosis factor receptor-associated factors (TRAFs) - a family of adaptor proteins that regulates life and death [J].
Arch, RH ;
Gedrich, RW ;
Thompson, CB .
GENES & DEVELOPMENT, 1998, 12 (18) :2821-2830
[3]   Lipoxins and novel 15-epi-lipoxin analogs display potent anti-inflammatory actions after oral administration [J].
Bannenberg, G ;
Moussignac, RL ;
Gronert, K ;
Devchand, PR ;
Schmidt, BA ;
Guilford, WJ ;
Bauman, JG ;
Subramanyam, B ;
Perez, HD ;
Parkinson, JF ;
Serhan, CN .
BRITISH JOURNAL OF PHARMACOLOGY, 2004, 143 (01) :43-52
[4]   Signal transduction by tumor necrosis factor and its relatives [J].
Baud, V ;
Karin, M .
TRENDS IN CELL BIOLOGY, 2001, 11 (09) :372-377
[5]   Adhesion molecule-dependent mechanisms regulate the rate of macrophage clearance during the resolution of peritoneal inflammation [J].
Bellingan, GJ ;
Xu, P ;
Cooksley, H ;
Cauldwell, H ;
Shock, A ;
Bottoms, S ;
Haslett, C ;
Mutsaers, SE ;
Laurent, GJ .
JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 196 (11) :1515-1521
[6]  
Bellingan GJ, 1996, J IMMUNOL, V157, P2577
[7]   The two NF-κB activation pathways and their role in innate and adaptive immunity [J].
Bonizzi, G ;
Karin, M .
TRENDS IN IMMUNOLOGY, 2004, 25 (06) :280-288
[8]   The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses [J].
Boone, DL ;
Turer, EE ;
Lee, EG ;
Ahmad, RC ;
Wheeler, MT ;
Tsui, C ;
Hurley, P ;
Chien, M ;
Chai, S ;
Hitotsumatsu, O ;
McNally, E ;
Pickart, C ;
Ma, A .
NATURE IMMUNOLOGY, 2004, 5 (10) :1052-1060
[9]   Homozygous C1q deficiency causes glomerulonephritis associated with multiple apoptotic bodies [J].
Botto, M ;
Dell'Agnola, C ;
Bygrave, AE ;
Thompson, EM ;
Cook, HT ;
Petry, F ;
Loos, M ;
Pandolfi, PP ;
Walport, MJ .
NATURE GENETICS, 1998, 19 (01) :56-59
[10]   Immune recognition of fungal β-glucans [J].
Brown, GD ;
Gordon, S .
CELLULAR MICROBIOLOGY, 2005, 7 (04) :471-479