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 Blood, 5 February 2009, Vol. 113, No. 6, pp. 1326-1331.
Prepublished online as a Blood First Edition Paper on December 10, 2008; DOI 10.1182/blood-2008-07-166660.

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PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS

BK channels in innate immune functions of neutrophils and macrophages

Kirill Essin1, Maik Gollasch1, Susanne Rolle1, Patrick Weissgerber2, Matthias Sausbier3, Erwin Bohn2, Ingo B. Autenrieth2, Peter Ruth3, Friedrich C. Luft1,4,*, William M. Nauseef46,*, and Ralph Kettritz1,*

1 Department of Nephrology, Campus-Virchow and Campus-Buch, Medical Faculty of the Charité, Experimental and Clinical Research Center at the Max Delbrück Center for Molecular Medicine, and HELIOS Kliniken Berlin, Berlin, Germany; 2 Institute of Medical Microbiology and Hygiene, University Hospital, Tübingen, Tübingen, Germany; 3 Department of Pharmacology and Toxicology, Institute of Pharmacy, University of Tübingen, Tübingen, Germany; 4 Inflammation Program and 5 Department of Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Coralville; and 6 VA Medical Center, Iowa City, IA

Oxygen-dependent antimicrobial activity of human polymorphonuclear leukocytes (PMNs) relies on the phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase to generate oxidants. As the oxidase transfers electrons from NADPH the membrane will depolarize and concomitantly terminate oxidase activity, unless there is charge translocation to compensate. Most experimental data implicate proton channels as the effectors of this charge compensation, although large-conductance Ca2+-activated K+ (BK) channels have been suggested to be essential for normal PMN antimicrobial activity. To test this latter notion, we directly assessed the role of BK channels in phagocyte function, including the NADPH oxidase. PMNs genetically lacking BK channels (BK–/–) had normal intracellular and extracellular NADPH oxidase activity in response to both receptor-independent and phagocytic challenges. Furthermore, NADPH oxidase activity of human PMNs and macrophages was normal after treatment with BK channel inhibitors. Although BK channel inhibitors suppressed endotoxin-mediated tumor necrosis factor-{alpha} secretion by bone marrow-derived macrophages (BMDMs), BMDMs of BK–/– and wild-type mice responded identically and exhibited the same ERK, PI3K/Akt, and nuclear factor-{kappa}B activation. Based on these data, we conclude that the BK channel is not required for NADPH oxidase activity in PMNs or macrophages or for endotoxin-triggered tumor necrosis factor-{alpha} release and signal transduction BMDMs.


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