Inflammatory resolution: New opportunities for drug discovery

被引:615
作者
Gilroy, DW
Lawrence, T
Perretti, M
Rossi, AG
机构
[1] St Bartholomews & Royal London Sch Med & Dent, William Harvey Res Inst, London EC1M 6BQ, England
[2] Univ Calif San Diego, Sch Med, Dept Pharmacol, Lab Gene Regulat & Signal Transduct, La Jolla, CA 92093 USA
[3] Univ Edinburgh, Sch Med, Ctr Inflammat Res, Resp Med Unit, Edinburgh EH8 9AG, Midlothian, Scotland
关键词
D O I
10.1038/nrd1383
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Treatment of inflammatory diseases today is largely based on interrupting the synthesis or action of mediators that drive the host's response to injury. Non-steroidal anti-inflammatories, steroids and antihistamines, for instance, were developed on this basis. Although such small-molecule inhibitors have provided the main treatment for inflammatory arthropathies and asthma, they are not without their shortcomings. This review offers an alternative approach to the development of novel therapeutics based on the endogenous mediators and mechanisms that switch off acute inflammation and bring about its resolution. It is thought that this strategy will open up new avenues for the future management of inflammation-based diseases.
引用
收藏
页码:401 / 416
页数:16
相关论文
共 149 条
[1]   Molecular mechanisms of glucocorticosteroid actions [J].
Adcock, IM .
PULMONARY PHARMACOLOGY & THERAPEUTICS, 2000, 13 (03) :115-126
[2]   Anti-inflammatory actions of the heme oxygenase-1 pathway [J].
Alcaraz, MJ ;
Fernandez, P ;
Guillén, MI .
CURRENT PHARMACEUTICAL DESIGN, 2003, 9 (30) :2541-2551
[3]   Retrovirally introduced prostaglandin D2 synthase suppresses lung injury induced by bleomycin [J].
Ando, M ;
Murakami, Y ;
Kojima, F ;
Endo, H ;
Kitasato, H ;
Hashimoto, A ;
Kobayashi, H ;
Majima, M ;
Inoue, M ;
Kondo, H ;
Kawai, S ;
Hayashi, I .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2003, 28 (05) :582-591
[4]  
Antoni C, 2002, CLIN EXP RHEUMATOL, V20, pS152
[5]   Annexin I is an endogenous ligand that mediates apoptotic cell engulfment [J].
Arur, S ;
Uche, UE ;
Rezaul, K ;
Fong, M ;
Scranton, V ;
Cowan, AE ;
Mohler, W ;
Han, DK .
DEVELOPMENTAL CELL, 2003, 4 (04) :587-598
[6]   IMMUNOSUPPRESSION BY GLUCOCORTICOIDS - INHIBITION OF NF-KAPPA-B ACTIVITY THROUGH INDUCTION OF I-KAPPA-B SYNTHESIS [J].
AUPHAN, N ;
DIDONATO, JA ;
ROSETTE, C ;
HELMBERG, A ;
KARIN, M .
SCIENCE, 1995, 270 (5234) :286-290
[7]   Cyclooxygenase-2-derived prostaglandin E2 and lipoxin A4 accelerate resolution of allergic edema in Angiostrongylus costaricensis-infected rats:: Relationship with concurrent eosinophilia [J].
Bandeira-Melo, C ;
Serra, MF ;
Diaz, BL ;
Cordeiro, RSB ;
Silva, PMR ;
Lenzi, HL ;
Bakhle, YS ;
Serhan, CN ;
Martins, MA .
JOURNAL OF IMMUNOLOGY, 2000, 164 (02) :1029-1036
[8]   Cutting edge:: Lipoxin (LX) A4 and aspirin-triggered 15-Epi-LXA4 block allergen-induced eosinophil trafficking [J].
Bandeira-Melo, C ;
Bozza, PT ;
Diaz, BL ;
Cordeiro, RSB ;
Jose, PJ ;
Martins, MA ;
Serhan, CN .
JOURNAL OF IMMUNOLOGY, 2000, 164 (05) :2267-2271
[9]  
Beer H D, 2000, Vitam Horm, V59, P217, DOI 10.1016/S0083-6729(00)59008-6
[10]   Biosynthesis of 15-deoxy-Δ12,14-PGJ2 and the litigation of PPARγ [J].
Bell-Parikh, LC ;
Ide, T ;
Lawson, JA ;
McNamara, P ;
Reilly, M ;
FitzGerald, GA .
JOURNAL OF CLINICAL INVESTIGATION, 2003, 112 (06) :945-955