Endogenous pro‐resolving and anti‐inflammatory lipid mediators: a new pharmacologic genus

British Journal of Pharmacology - Tập 153 Số S1 - 2008
Charles N. Serhan1,2, Nan Chiang1
1Department of Anesthesiology, Center for Experimental Therapeutics and Reperfusion Injury, Perioperative and Pain Medicine, Brigham and Women's Hospital, Boston, MA, USA
2Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Harvard Medical School, Boston, MA, USA

Tóm tắt

Complete resolution of an acute inflammatory response and its return to homeostasis are essential for healthy tissues. Here, we overview ongoing efforts to characterize cellular and molecular mechanisms that govern the resolution of self‐limited inflammation. Systematic temporal analyses of evolving inflammatory exudates using mediator lipidomics‐informatics, proteomics, and cellular trafficking with murine resolving exudates demonstrate novel endogenous pathways of local‐acting mediators that share both anti‐inflammatory and pro‐resolving properties. In murine systems, resolving‐exudate leukocytes switch their phenotype to actively generate new families of mediators from major omega‐3 fatty acids EPA and DHA termed resolvins and protectins. Recent advances on their biosynthesis and actions are reviewed with a focus on the E‐series resolvins (RvE1, RvE2), D series resolvins (RvD1, RvD2) and the protectins including neuroprotectin D1/protectin D1 (NPD1/PD1) as well as their aspirin‐triggered epimeric forms. Members of each new family demonstrate potent stereo‐specific actions, joining the lipoxins as endogenous local signals that govern resolution and endogenous anti‐inflammation mechanisms. In addition to their origins and roles in resolution biology in the immune system, recent findings indicate that these new mediator families also display potent protective actions in lung, kidney, and eye as well as enhance microbial clearance. Thus, these endogenous agonists of resolution pathways constitute a novel genus of chemical mediators that possess pro‐resolving, anti‐inflammatory, and antifibrotic as well as host‐directed antimicrobial actions. These may be useful in the design of new therapeutics and treatments for diseases with the underlying trait of uncontrolled inflammation and redox organ stress.

British Journal of Pharmacology (2008) 153, S200–S215; doi:10.1038/sj.bjp.0707489; published online 29 October 2007

Từ khóa


Tài liệu tham khảo

10.1074/jbc.M509796200

10.1084/jem.20042031

10.1016/j.bbrc.2005.07.181

10.1074/jbc.M603766200

10.4049/jimmunol.178.6.3912

10.1073/pnas.0409271102

10.4049/jimmunol.164.2.1029

10.1038/sj.bjp.0705912

10.4049/jimmunol.174.7.4345

10.1038/35037026

Bazan NG, 1990, Nutrition and the Brain, 1

Bazan NG, 1992, Supply, uptake, and utilization of docosahexaenoic acid during photoreceptor cell differentiation, Nestle Nutr Workshop Ser, 28, 121

Bergström S, 1982, Les Prix Nobel: Nobel Prizes, Presentations, Biographies and Lectures, 129

10.1161/CIRCULATIONAHA.106.629907

Borgeat P, 1976, Transformation of arachidonic acid and homo‐gamma‐linolenic acid by rabbit polymorphonuclear leukocytes, J Biol Chem, 251, 7816, 10.1016/S0021-9258(19)57008-9

10.1016/S0021-9258(20)78281-5

10.1096/fj.07-8473com

10.1073/pnas.0405445101

10.1172/JCI7016

10.1124/pr.58.3.4

10.1038/sj.bjp.0705220

10.1054/plef.2002.0457

10.1164/ajrccm/145.6.1281

10.1073/pnas.92.21.9475

10.1073/pnas.96.14.8247

10.1006/bbrc.2001.5841

10.1006/bbrc.1999.1732

10.1038/nm1591

Cotran RS, 1999, Robbins Pathologic Basis of Disease, 1425

10.1038/nature01322

10.1096/fj.04-2565com

10.4049/jimmunol.177.9.5902

10.1001/jama.291.5.585

10.1124/jpet.300.2.385

10.1073/pnas.0404722101

10.1038/sj.bjp.0706506

10.4049/jimmunol.168.10.5260

10.1016/j.plefa.2005.05.007

10.1038/9550

10.1038/nrd1383

10.1016/j.coph.2005.02.006

GISSI‐Prevenzione Investigators(1999).Dietary supplementation withn−3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI‐Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico.Lancet354:447–455.

10.1074/jbc.M410638200

10.1021/jm030569l

10.1084/jem.189.12.1923

10.1016/S0021-9258(18)99432-9

Hansen HS, 1974, Inhibition by indomethacin and aspirin of 15‐hydroxyprostaglandin dehydrogenase in vitro, Prostaglandins Leukot Essent Fatty Acids, 8, 95

10.1146/annurev.pathol.1.110304.100100

10.1016/j.biopha.2006.06.023

10.1096/fj.05-4724fje

10.1038/ni1205-1179

10.1074/jbc.M300218200

10.1016/j.jasms.2006.09.002

10.1016/j.prostaglandins.2005.04.004

10.1213/01.ane.0000252414.00363.c4

JinY AritaM ZhangQ SerhanC DanaR(2007).Aspirin‐triggered lipoxin agonist (ATLa) inhibits corneal angiogenesis (abstract).Association for Research in Vision and Ophthalmology Annual Meeting Fort Lauderdale May 6–10 2007.

10.1038/ni1056

Katoh T, 1992, Renal hemodynamic actions of lipoxins in rats: a comparative physiological study, Am J Physiol, 263, F436

10.1111/j.1523-1755.2004.00487.x

Lands WEM, 1987, Proceedings of the AOCS Short Course on Polyunsaturated Fatty Acids and Eicosanoids

10.1016/j.tips.2007.02.003

10.1038/nature03491

10.1172/JCI111612

10.1097/01.ASN.0000015795.74094.91

10.1038/89759

10.1038/nm748

10.4049/jimmunol.178.1.496

10.1096/fj.07-8653com

10.1038/scientificamerican0502-46

10.1100/tsw.2006.118

10.1194/jlr.D400020-JLR200

10.1172/JCI25420

10.1089/ten.2007.0100

10.1038/ni1275

10.1096/fasebj.12.6.487

10.1074/jbc.272.11.6972

10.1084/jem.183.1.137

10.1016/j.plefa.2005.05.004

Majno G, 1996, Cells, Tissues and Disease: Principles of General Pathology

10.1074/jbc.M305841200

10.1161/01.CIR.0000014682.14181.F2

10.1097/01.ASN.0000032417.73640.72

10.1073/pnas.0402531101

10.1038/nature01320

10.1084/jem.20040566

10.1038/nm786

10.1016/j.plefa.2005.05.020

10.1021/bi992551b

10.1021/bi992000l

10.1016/j.tetlet.2004.09.129

Romano M, 1996, Activation of human monocytes and the acute monocytic leukemia cell line (THP‐1) by lipoxins involves unique signaling pathways for lipoxin A4 versus lipoxin B4, J Immunol, 157, 2149, 10.4049/jimmunol.157.5.2149

Rossi AG, 2007, Progress in Inflammation Research

10.1038/nm1468

10.1007/s11745-001-0805-6

Samuelsson B, 1982, Les Prix Nobel: Nobel Prizes, Presentations, Biographies and Lectures, 153

10.1126/science.6301011

10.1126/science.2820055

10.1046/j.1471-4159.1994.62062437.x

10.1016/j.bbrc.2006.08.179

10.1073/pnas.94.18.9967

10.4049/jimmunol.169.12.7063

10.1038/nature05877

10.1016/0005-2760(94)90185-6

10.1016/S0090-6980(97)00001-4

10.1016/S0090-6980(02)00047-3

10.1007/s00418-004-0695-8

10.1146/annurev.immunol.25.022106.141647

10.1096/fj.06-7227rev

10.1084/jem.192.8.1197

10.4049/jimmunol.176.3.1848

10.1016/j.plefa.2005.07.001

10.1084/jem.20020760

10.1208/aapsj080233

10.4049/jimmunol.171.12.6856

10.1021/bi00044a041

10.1038/ni1276

10.1080/07315724.1999.10718888

10.1074/jbc.M609212200

10.1084/jem.20061826

10.1172/JCI1578

10.1084/jem.185.9.1693

10.1016/j.chembiol.2006.09.011

10.1016/S0167-4889(00)00039-2

10.1096/fj.00-0836fje

Vane JR, 1982, Les Prix Nobel: Nobel Prizes, Presentations, Biographies and Lectures, 181

10.1016/S0021-9258(18)91081-1

10.1096/fj.06-5809com

10.1016/S0165-6147(03)00166-4

Winyard PG, 2003, Methods in Molecular Biology, 378

10.1016/j.plefa.2006.12.006

Thông tin
Thông tin xuất bản

British Journal of Pharmacology

Tập 153 Số S1

Thông tin tác giả