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Extracellular DNA Traps by Basophils Independent Formation Of NADPH Oxidase−Independent Formation of Extracellular DNA Traps by Basophils Mahbubul Morshed, Ruslan Hlushchuk, Dagmar Simon, Andrew F. Walls, Kazushige Obata-Ninomiya, Hajime This information is current as Karasuyama, Valentin Djonov, Alexander Eggel, Thomas of September 26, 2021. Kaufmann, Hans-Uwe Simon and Shida Yousefi J Immunol 2014; 192:5314-5323; Prepublished online 25 April 2014; doi: 10.4049/jimmunol.1303418 Downloaded from http://www.jimmunol.org/content/192/11/5314 Supplementary http://www.jimmunol.org/content/suppl/2014/04/25/jimmunol.130341 Material 8.DCSupplemental http://www.jimmunol.org/ References This article cites 43 articles, 14 of which you can access for free at: http://www.jimmunol.org/content/192/11/5314.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 26, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *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 © 2014 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology NADPH Oxidase–Independent Formation of Extracellular DNA Traps by Basophils Mahbubul Morshed,* Ruslan Hlushchuk,† Dagmar Simon,‡ Andrew F. Walls,x Kazushige Obata-Ninomiya,{ Hajime Karasuyama,{,‖ Valentin Djonov,† Alexander Eggel,# Thomas Kaufmann,* Hans-Uwe Simon,* and Shida Yousefi* Basophils are primarily associated with a proinflammatory and immunoregulatory role in allergic diseases and parasitic infections. Recent studies have shown that basophils can also bind various bacteria both in the presence and the absence of opsonizing Abs. In this report, we show that both human and mouse basophils are able to produce mitochondrial reactive oxygen species and to form extracellular DNA traps upon IL-3 priming and subsequent activation of the complement factor 5 a receptor or Fc«RI. Such basophil extracellular traps (BETs) contain mitochondrial, but not nuclear DNA, as well as the granule proteins basogranulin and mouse mast cell protease 8. BET formation occurs despite the absence of any functional NADPH oxidase in basophils. BETs can be Downloaded from found in both human and mouse inflamed tissues, suggesting that they also play a role under in vivo inflammatory conditions. Taken together, these findings suggest that basophils exert direct innate immune effector functions in the extracellular space. The Journal of Immunology, 2014, 192: 5314–5323. asophils make up ,0.5% of all peripheral blood leuko- types at sites of allergic inflammation. IL-3 is not only an im- http://www.jimmunol.org/ cytes but share with mast cells the unique capacity to portant activation factor for basophils, it is also important for their B synthesize various hallmark mediators of allergic in- differentiation and survival (4). In addition, IL-3 primes basophils flammation and to express high-affinity IgE receptors (FcεRI) (1). to produce lipid mediators, such as leukotriene C4 (LTC4)inan Aggregation of FcεRI bound to IgE by multivalent Ag leads to allergen-independent manner in response to stimulation with basophil activation, granule exocytosis, and mediator release. complement factor 5 (C5a) (4). It also has been shown that thymic Besides functioning as effector cells, basophils also may play an stromal lymphopoietin (TSLP) can act as a key regulator of ba- important role in the initiation of an allergic inflammatory re- sophil hematopoiesis, independent of IL-3 (5). sponse (e.g., by recruiting other inflammatory cells) (2, 3). A role for basophils in innate immunity is suggested by their Basophils are also a prime source for the Th2 cytokines IL-4 and expression of the functional TLRs 2 and 4 as well as by the by guest on September 26, 2021 IL-13 (1). The phenotype and functions of human basophils are possibility of activating these cells by multiple proteases, including tightly regulated by IL-3, a cytokine produced by various cell Der p1 and hookworm, in a non–IgE-dependent manner (6, 7). Basophils also can recognize microbes in an IgE-dependent manner (8) and release antibacterial factors, such as b-defensin *Institute of Pharmacology, University of Bern, CH-3010 Bern, Switzerland; and cathelicidin (9). Previously published work has demonstrated †Institute of Anatomy, University of Bern, CH-3012 Bern, Switzerland; ‡Department of Dermatology, Inselspital, Bern University Hospital, CH-3010 Bern, Switzerland; that both neutrophils and eosinophils are capable of killing bac- x Immunopharmacology Group, University of Southampton, Southampton General teria extracellularly by forming DNA traps, so-called neutrophil Hospital, Southampton SO16 6YD, United Kingdom; {Department of Immune Regulation, Tokyo Medical and Dental University Graduate School of Medical and extracellular traps (NETs) and eosinophil extracellular traps (EETs) Dental Sciences, Tokyo 113-8518, Japan; ‖Core Research for Evolutional Science (10, 11). In this study, we have investigated whether basophils also and Technology, Japan Science and Technology Agency, Tokyo 113-8518, Japan; can form extracellular DNA traps. and #Institute of Immunology, University of Bern, Inselspital, CH-3010 Bern, Switzerland Received for publication December 23, 2013. Accepted for publication March 31, Materials and Methods 2014. Reagents This work was supported by the Swiss National Science Foundation. M.M. is a Ph.D. Recombinant human IL-3, rat IgG2a, rabbit IgG, as well as recombinant student of the Graduate School of Cellular and Biomedical Sciences of the University of Bern. Images were acquired on equipment supported by the Microscopy Imaging human eotaxin and thymic stromal lymphopoietin (TSLP) were from R&D Centre of the University of Bern. Systems Europe (Abingdon, U.K.). GM-CSF was provided by Novartis Pharma (Nurnberg,€ Germany). Human and mouse C5a were purchased Address correspondence and reprint requests to Dr. Shida Yousefi, Institute of Phar- from Hycult Biotech (Uden, The Netherlands). LPS, dihydrorhodamine- macology, University of Bern, Friedbuehlstrasse 49, CH-3010 Bern, Switzerland. E-mail address: shida.yousefi@pki.unibe.ch 123 (DHR), NBT, and fMLF, as well as Luria–Bertani and BHI media were obtained from Sigma-Aldrich (Buchs, Switzerland). Lipoteichoic The online version of this article contains supplemental material. acid (LTA) was a gift from Dr. T. Hartung (University of Konstanz, Abbreviations used in this article: BET, basophil extracellular trap; BG, basogranu- Konstanz, Germany). Platelet-activating factor (PAF) was from Millipore lin; C5a, complement factor 5a; DHR, dihydrorhodamine-123; DNase, deoxyribonu- (Zug, Switzerland). Diphenylene iodonium chloride (DPI) and PMA were clease; DPI, diphenylene iodonium chloride; EET, eosinophil extracellular trap; from Calbiochem (Merck, Darmstadt, Germany). Mitoquinone (MitoQ) EthD-1, ethidium homodimer-1; i.d., intradermal(ly); LTA, lipoteichoic acid; MitoQ, was from Biotrend Chemicals (Zurich, Switzerland). Propidium iodide mitoquinone; mMCP-8, mouse mast cell protease 8; MMP-9, matrix metallopepti- (PI), Hoechst 33342, SYTO13, MitoSOX Red, mounting medium con- dase 9; mtDNA, mitochondrial DNA; nDNA, nuclear DNA; NET, neutrophil extra- cellular trap; NOX, NADPH oxidase; PAF, platelet-activating factor; phox, taining DAPI, as well as calcein-AM and ethidium homodimer-1 (EthD-1), phagocytic oxidase; PI, propidium iodide; qPCR, quantitative PCR; ROS, reactive HBSS, and RPMI 1640 medium were from Invitrogen (Paisley, U.K.). oxygen species; TNP, 2,4,6-trinitrophenyl; TSLP, thymic stromal lymphopoietin. X-VIVO 15 medium was from Lonza (Verviers, Belgium). Anti-FcεRIa Ab (CRA1) was from Miltenyi Biotec (Bergisch Gladbach, Germany). APC- Copyright Ó 2014 by The American Association of Immunologists, Inc. 0022-1767/14/$16.00 conjugated anti-human FcεR1a (CRA1) and FITC-conjugated anti-human www.jimmunol.org/cgi/doi/10.4049/jimmunol.1303418 The Journal of Immunology 5315 IgE (clone Ige21) Abs were from eBioscience (Vienna, Austria). FITC- formaldehyde-fixed and paraffin-embedded human and mouse skin sec- conjugated anti-mouse FcεRIa (clone MAR-1), rat anti-mouse mast cell tions, respectively, using appropriate secondary Abs labeled with Alexa protease 8 (mMCP-8, TUG8), APC-conjugated anti-mouse c-kit (CD117, Fluor 488 (Invitrogen). After washing with PBS, the specimens were clone 2B8), APC-conjugated anti-mouse Gr-1 (Ly-6G/Ly-6C, clone mounted in a drop of fluorescence mounting medium (DakoCytomation, RB6-8C5), and APC-conjugated goat anti-rat Abs were from BioLegend Glostrup, Denmark). Slides were analyzed by confocal laser scanning (Lucerna-Chem, Luzern, Switzerland). Anti-rabbit matrix metallopeptidase microscopy (LSM 510; Carl Zeiss Micro Imaging, Jena, Germany). 9 (MMP-9) Ab was purchased from Abcam (Cambridge, U.K.). Anti-mouse gp91phox (clone 53/gp91[phox]), APC-conjugated anti-human CCR3 Electron microscopy (CD193, clone 5E8), and PE-conjugated anti–IL-3Ra (CD123, clone 9F5) Abs were obtained from BD Biosciences
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