Resolution of in flammation: state of the art, definitions and terms

A recent focus meeting on Controlling Acute Inflammation was held in London, April 27–28, 2006, organized by D.W. Gilroy and S.D. Brain for the British Pharmacology Society. We concluded at the meeting that a consensus report was needed that addresses the rapid progress in this emerging field and details how the specific study of resolution of acute inflammation provides leads for novel anti‐inflammatory therapeutics, as well as defines the terms and key components of interest in the resolution process within tissues as appreciated today. The inflammatory response protects the body against infection and injury but can itself become dysregulated with deleterious consequences to the host. It is now evident that endogenous biochemical pathways activated during defense reactions can counter‐regulate inflammation and promote resolution. Hence, resolution is an active rather than a passive process, as once believed, which now promises novel approaches for the treatment of inflammation‐associated diseases based on endogenous agonists of resolution.—Serhan, C. N., Brain, S. D., Buckley, C. D., Gilroy, D. W., Haslett, C., O'Neill, L. A. J., Perretti, M., Rossi, A. G., Wallace, J. L. Resolution of inflammation: state of the art, definitions and terms. FASEB J. 21, 325–332 (2007)

[1]  Charles N. Serhan,et al.  Molecular circuits of resolution: formation and actions of resolvins and protectins , 2005, The Journal of Immunology.

[2]  G. Prestwich,et al.  Regulation of lung injury and repair by Toll-like receptors and hyaluronan , 2005, Nature Medicine.

[3]  F. Liew,et al.  Toll-like receptor 2 signaling modulates the functions of CD4+ CD25+ regulatory T cells. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[4]  M. Perretti,et al.  Modulation of Phagocytosis of Apoptotic Neutrophils by Supernatant from Dexamethasone-Treated Macrophages and Annexin-Derived Peptide Ac2–261 , 2005, The Journal of Immunology.

[5]  G. Majno,et al.  Cells, tissues, and disease : principles of general pathology , 1996 .

[6]  C. Serhan,et al.  Resolvins , 2002, The Journal of experimental medicine.

[7]  Adriano G. Rossi,et al.  Inflammatory Resolution: new opportunities for drug discovery , 2004, Nature Reviews Drug Discovery.

[8]  F. Martinon,et al.  Gout-associated uric acid crystals activate the NALP3 inflammasome , 2006, Nature.

[9]  G. Weissmann,et al.  Release of inflammatory mediators from stimulated neutrophils. , 1980, The New England journal of medicine.

[10]  Shubhada Sankararaman,et al.  Cells, Tissues, and Disease: Principles of General Pathology , 2005 .

[11]  D. Gilroy,et al.  Inducible cyclooxygenase may have anti-inflammatory properties , 1999, Nature Medicine.

[12]  S. Robbins,et al.  Pathologic basis of disease , 1974 .

[13]  M. Perretti Endogenous mediators that inhibit the leukocyte-endothelium interaction. , 1997, Trends in pharmacological sciences.

[14]  C. Serhan A search for endogenous mechanisms of anti-inflammation uncovers novel chemical mediators: missing links to resolution , 2004, Histochemistry and Cell Biology.

[15]  M. Teixeira,et al.  Phosphoinositide‐3 kinases critically regulate the recruitment and survival of eosinophils in vivo: importance for the resolution of allergic inflammation , 2005, Journal of leukocyte biology.

[16]  C. Haslett,et al.  Glucocorticoid Augmentation of Macrophage Capacity for Phagocytosis of Apoptotic Cells Is Associated with Reduced p130Cas Expression, Loss of Paxillin/pyk2 Phosphorylation, and High Levels of Active Rac1 , 2001, The Journal of Immunology.

[17]  M. Salmon,et al.  A stromal address code defined by fibroblasts. , 2005, Trends in immunology.

[18]  G. Chejfec Robbins Pathologic Basis of Disease , 2009 .

[19]  S. Marullo,et al.  Endogenous lipid- and peptide-derived anti-inflammatory pathways generated with glucocorticoid and aspirin treatment activate the lipoxin A4 receptor , 2002, Nature Medicine.

[20]  B. Cronstein Going with the flow: methotrexate, adenosine, and blood flow , 2006, Annals of the rheumatic diseases.

[21]  N. Niles Pathologic Basis of Disease , 1974 .

[22]  J. Lord,et al.  Fibroblasts regulate the switch from acute resolving to chronic persistent inflammation. , 2001, Trends in immunology.

[23]  John Savill,et al.  Resolution of inflammation: the beginning programs the end , 2005, Nature Immunology.

[24]  Charles N. Serhan,et al.  Lipid mediator class switching during acute inflammation: signals in resolution , 2001, Nature Immunology.

[25]  T. Lawrence,et al.  Antiinflammatory effects of dexamethasone are partly dependent on induction of dual specificity phosphatase 1 , 2006, The Journal of experimental medicine.

[26]  F. Liew,et al.  Negative regulation of Toll-like receptor-mediated immune responses , 2005, Nature Reviews Immunology.

[27]  L. Joosten,et al.  Toll-like receptor 2 controls expansion and function of regulatory T cells. , 2006, The Journal of clinical investigation.

[28]  J. M. Cousin,et al.  Glucocorticoids promote nonphlogistic phagocytosis of apoptotic leukocytes. , 1999, Journal of immunology.

[29]  A. Filer,et al.  Targeting the stromal microenvironment in chronic inflammation. , 2006, Current opinion in pharmacology.

[30]  Christopher Haslett,et al.  Cyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis , 2006, Nature Medicine.

[31]  James E. Evans,et al.  Molecular identification of a danger signal that alerts the immune system to dying cells , 2003, Nature.

[32]  F. Martinon,et al.  NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder. , 2004, Immunity.

[33]  P. Colville-Nash,et al.  The involvement of the apoptosis-modulating proteins ERK 1/2, Bcl-xL and Bax in the resolution of acute inflammation in vivo. , 2006, The American journal of pathology.

[34]  L. O’Neill,et al.  TLRs, NLRs and RLRs: a trinity of pathogen sensors that co-operate in innate immunity. , 2006, Trends in immunology.

[35]  M. Perretti,et al.  Spatial and Temporal Profiles for Anti-Inflammatory Gene Expression in Leukocytes during a Resolving Model of Peritonitis , 2006 .