NADPH oxidase-independent formation of extracellular DNA traps by basophils.
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 FcεRI. 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 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.
Institute of Pharmacology, University of Bern, CH-3010 Bern, Switzerland;
Mahbubul
M
Morshed
Institute of Anatomy, University of Bern, CH-3012 Bern, Switzerland;
Ruslan
R
Hlushchuk
Department of Dermatology, Inselspital, Bern University Hospital, CH-3010 Bern, Switzerland;
Dagmar
D
Simon
Immunopharmacology Group, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, United Kingdom;
Andrew F
AF
Walls
Department of Immune Regulation, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, Tokyo 113-8518, Japan;
Kazushige
K
Obata-Ninomiya
Department of Immune Regulation, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, Tokyo 113-8518, Japan; Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Tokyo 113-8518, Japan; and.
Hajime
H
Karasuyama
Institute of Anatomy, University of Bern, CH-3012 Bern, Switzerland;
Valentin
V
Djonov
Institute of Immunology, University of Bern, Inselspital, CH-3010 Bern, Switzerland.
Alexander
A
Eggel
Institute of Pharmacology, University of Bern, CH-3010 Bern, Switzerland;
Thomas
T
Kaufmann
Institute of Pharmacology, University of Bern, CH-3010 Bern, Switzerland;
Hans-Uwe
HU
Simon
Institute of Pharmacology, University of Bern, CH-3010 Bern, Switzerland; shida.yousefi@pki.unibe.ch.
Shida
S
Yousefi
D000818:Animals; D001491:Basophils / Q000276:immunology*; D003182:Complement C5 / Q000276:immunology; D004247:DNA / Q000276:immunology*; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D007377:Interleukin-3 / Q000276:immunology; D008297:Male; D051379:Mice; D019255:NADPH Oxidases / Q000276:immunology*; D017455:Receptors, IgE / Q000276:immunology; D053802:Tryptases / Q000276:immunology
D003182:Complement C5; C508596:IL3 protein, human; D007377:Interleukin-3; D017455:Receptors, IgE; D004247:DNA; D019255:NADPH Oxidases; D053802:Tryptases