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Cutting Edge: Lipoxins Rapidly Stimulate Nonphlogistic Cutting Edge: Lipoxins Rapidly Stimulate Nonphlogistic Phagocytosis of Apoptotic Neutrophils by Monocyte-Derived Macrophages This information is current as of September 29, 2021. Catherine Godson, Siobhan Mitchell, Killeen Harvey, Nicos A. Petasis, Nancy Hogg and Hugh R. Brady J Immunol 2000; 164:1663-1667; ; doi: 10.4049/jimmunol.164.4.1663 http://www.jimmunol.org/content/164/4/1663 Downloaded from References This article cites 31 articles, 16 of which you can access for free at: http://www.jimmunol.org/content/164/4/1663.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 29, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2000 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. ● Cutting Edge: Lipoxins Rapidly Stimulate Nonphlogistic Phagocytosis of Apoptotic Neutrophils by Monocyte-Derived Macrophages1 Catherine Godson,2,3* Siobhan Mitchell,2* Killeen Harvey,* Nicos A. Petasis,† Nancy Hogg,‡ and Hugh R. Brady* gests that neutrophil-mediated tissue damage is limited by polymor- Downloaded from Lipoxins (LX) are lipoxygenase-derived eicosanoids generated phonuclear neutrophil (PMN)4 apoptosis and subsequent phagocyto- during inflammation. LX inhibit polymorphonuclear neutrophil sis by macrophages (M␾) and other “nonprofessional” phagocytes. It (PMN) chemotaxis and adhesion and are putative braking signals is noteworthy that such phagocytic clearance is nonphlogistic; i.e., in for PMN-mediated tissue injury. In this study, we report that contrast to phagocytosis of particles opsonized with complement or LXA4 promotes another important step in the resolution phase of Ig, phagocytosis of apoptotic leukocytes does not provoke the release inflammation, namely, phagocytosis of apoptotic PMN by mono- of proinflammatory mediators (reviewed in Refs. 1 and 2). These http://www.jimmunol.org/ ␾ cyte-derived macrophages (M ). LXA4 triggered rapid, concen- observations suggest the existence of a specialized phagocytic process tration-dependent uptake of apoptotic PMN. This bioactivity was for removal of apoptotic PMN from an inflammatory milieu. Several shared by stable synthetic LXA4 analogues (picomolar concen- aspects of phagocyte-apoptotic cell recognition systems have been trations) but not by other eicosanoids tested. LXA4-triggered described involving the concerted action of cell surface molecules phagocytosis did not provoke IL-8 or monocyte chemoattractant (reviewed in Refs. 1–3). To date, rapid modulation of PMN phago- protein-1 release. LXA4-induced phagocytosis was attenuated by cytosis has not been described (4, 5). ␣ ␤ anti-CD36, v 3, and CD18 mAbs. LXA4-triggered PMN uptake Lipoxins (lipoxygenase interaction products; LX) are lipid-derived was inhibited by pertussis toxin and by 8-bromo-cAMP and was mediators typically generated by transcellular lipoxygenation of ara- chidonic acid. Several lines of evidence suggest that LX are braking by guest on September 29, 2021 mimicked by Rp-cAMP, a protein kinase A inhibitor. LXA4 at- ␾ signals for PMN recruitment in host defense, inflammation, and hy- tenuated PGE2-stimulated protein kinase A activation in M . persensitivity reactions (reviewed in Ref. 6). LX have been detected These results suggest that LXA4 is an endogenous stimulus for PMN clearance during inflammation and provide a novel ratio- in tissues and inflammatory exudates in experimental and human dis- ␤ nale for using stable synthetic analogues as anti-inflammatory eases. LX, at nanomolar concentrations, inhibit PMN chemotaxis, 2 compounds in vivo. The Journal of Immunology, 2000, 164: integrin and P-selectin-dependent PMN adhesion to endothelial cells, and PMN transmigration across confluent monolayers of endothelial 1663–1667. and epithelial cells in vitro in response to leukotrienes and other in- flammatory mediators (6–8). LX inhibit several other proinflamma- t is increasingly appreciated that the resolution of inflamma- tory responses of leukocytes and parenchymal cells, including PMN tion is a dynamically regulated process. Of particular rele- degranulation and cytokine release by colonic epithelial cells (9, 10). Furthermore, ex vivo treatment of PMN with LXA blunts their sub- I vance in this context is the clearance of accumulated leukocytes 4 (1, 2). Evidence from in vitro models and from histopathology sug- sequent recruitment to inflamed renal glomeruli in experimental im- mune complex glomerulonephritis, and impaired LXA4 biosynthesis has been associated with exaggerated PMN recruitment in the latter *Centre for Molecular Inflammation and Vascular Research, Mater Misericordiae setting (11). Interestingly, the topical and systemic administration of Hospital and Department of Medicine and Therapeutics, Conway Institute of Biomo- lecular and Biomedical Research, University College Dublin, Dublin, Ireland; †De- LX and/or synthetic LX analogues inhibits PMN recruitment and partment of Chemistry, University of Southern California, Los Angeles, CA 90089; plasma exudation induced by leukotriene B4 and other insults in var- and ‡Imperial Cancer Research Fund, London, United Kingdom ious models of acute inflammation (12, 13). Aspirin promotes the Received for publication October 13, 1999. Accepted for publication December generation of LX epimers during leukocyte interactions with endo- 17, 1999. thelial and epithelial cells which may account for some of the efficacy The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. 1 This research was funded by grants from the Health Research Board, the Wellcome Trust, Forbairt (Enterprise Ireland) a President’s Research Award from University 3 Address correspondence and reprint requests to Dr. Catherine Godson, Department College Dublin, and the Mater College. The results were presented in preliminary of Medicine and Therapeutics, University College Dublin, 41 Eccles Street, Dublin 7, form at the 31st and 32nd Annual Meetings of the American Society of Nephrology Ireland. E-mail address: [email protected] and published in abstract form in J. Am. Soc. Nephrol. 1998; 9:482A and J. Am. Soc. 4 Abbreviations used in this paper: PMN, polymorphonuclear neutrophil; M␾, mac- Nephrol. 1999; 10: 532A. rophage; LX, lipoxin; PKA, protein kinase A; MPO, myleoperoxidase; MCP-1. 2 C.G. and S.M. contributed equally to this work. monocyte chemoattractant protein-1; PTX, pertussis toxin. Copyright © 2000 by The American Association of Immunologists 0022-1767/00/$02.00 ● 1664 CUTTING EDGE Downloaded from http://www.jimmunol.org/ by guest on September 29, 2021 ␾ FIGURE 1. LXA4 rapidly stimulates nonphlogistic phagocytosis of apoptotic PMN by M . A, Dual laser flow cytometry demonstrating progression of PMN from normal (gate C) through early apoptotic (gate D) to late apoptotic/secondary necrotic (gate M) phases during aging for4h(left), 24 h (middle), and 48 h (right) (14). For ␾ ␾ Ϫ9 M phagocytosis assays, PMN were aged for 24 h. B, Exposure of M to LXA4 (10 M, 15 min) enhances their phagocytosis of apoptotic PMN during a 30-min coincubation at 37°C. As a positive control in parallel experiments, M␾ were pretreated with anti-CD44 mAb (J-173, 80 ␮g/ml, 20 min, 22°C). Data are means Ϯ SEM and are expressed as percent M␾ staining positively for MPO (n ϭ 10, p Ͻ 0.01). C, IL-8 release from M␾-PMN coincubations. IL-8 was determined by ELISA (R&D ␾ ␾ ␾ Systems) of supernatants harvested after 30 min from M cultures, cocultures of aged PMN with M pretreated with LXA4 (1 nM) or vehicle (15 min), or M exposed to opsonized zymosan (10 mg/ml). Data are means Ϯ SEM (n ϭ 5) and are expressed as percent zymosan-stimulated IL-8 release. of this classic nonsteroidal anti-inflammatory agent (6, 12–15). To- bination of light microscopy and dual laser flow cytometry (Epics Elite gether these observations raise the possibility that the LX play dy- flow cytometer, Coulter, Hialeah, FL) using Hoechst 33342 and propidium namic roles in the resolution phase of PMN-mediated inflammation. iodide (16). In this study, we further expand on the anti-inflammatory ac- M␾ phagocytosis of apoptotic PMN tions of LX by determining their effects on M␾ phagocytosis of ␾ apoptotic PMN. We demonstrate that exposure of M␾ to LX M were exposed to experimental stimuli, washed with RPMI 1640, and coin- cubated with aged PMN in 24-well tissue culture plates (4 ϫ 106 PMN/ml RPMI causes rapid enhancement of phagocytosis of apoptotic PMN; this 1640/well) at 37°C for 30 min. After coincubation, the cells were washed with response is concentration dependent, involves multiple adhesion PBS, fixed with 2.5% glutaraldehyde, and stained for myeloperoxidase (MPO) molecules, can be mimicked by stable synthetic LX analogues, and activity with dimethoxybenzidine
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