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BK channels in innate immune functions of neutrophils and macrophages

Kirill Essin1, Maik Gollasch, Susanne Rolle

  • 1Department of Nephrology, Campus-Virchow, Medical Faculty of the Charité, Experimental and Clinical Research Center at the Max Delbrück Center for Molecular Medicine, Berlin, Germany.

Blood
|December 17, 2008
PubMed

Insights

Large-conductance Ca2+-activated K+ (BK) channels are not essential for the antimicrobial function of human phagocytes. Studies show normal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity in BK channel-deficient cells and after inhibitor treatment.

Area of Science:

  • Immunology
  • Cell Physiology
  • Molecular Biology

Background:

  • Human polymorphonuclear leukocytes (PMNs) depend on nicotinamide adenine dinucleotide phosphate (NADPH) oxidase for oxygen-dependent antimicrobial activity.
  • Phagocyte membrane depolarization during NADPH oxidase activity necessitates charge compensation, with proton channels often implicated.
  • Large-conductance Ca2+-activated K+ (BK) channels have been proposed as crucial for PMN antimicrobial function.

Purpose of the Study:

  • To investigate the specific role of BK channels in phagocyte function, particularly in relation to NADPH oxidase activity.
  • To determine if BK channels are essential for normal antimicrobial activity in human PMNs and macrophages.

Main Methods:

  • Assessed NADPH oxidase activity in PMNs genetically lacking BK channels (BK(-/-)) under various challenges.
  • Evaluated NADPH oxidase activity in human PMNs and macrophages treated with BK channel inhibitors.
  • Examined endotoxin-mediated tumor necrosis factor-alpha secretion and associated signaling pathways (ERK, PI3K/Akt, NF-κB) in BK(-/-) and wild-type bone marrow-derived macrophages (BMDMs).

Main Results:

  • PMNs lacking BK channels exhibited normal intracellular and extracellular NADPH oxidase activity.
  • Human PMNs and macrophages showed unimpaired NADPH oxidase activity following BK channel inhibitor treatment.
  • BK channel inhibitors reduced TNF-α secretion, but BK(-/-) and wild-type BMDMs displayed identical activation of ERK, PI3K/Akt, and NF-κB pathways.

Conclusions:

  • The BK channel is not required for NADPH oxidase activity in human PMNs and macrophages.
  • BK channels are dispensable for endotoxin-triggered tumor necrosis factor-alpha release and associated signal transduction in BMDMs.
  • These findings challenge the notion that BK channels are essential for phagocyte antimicrobial functions.

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