Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 106, Issue 18, Pages 7642-7647Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0902761106
Keywords
HV1(-/-); immunity; voltage-gated ion channel; innate immunity
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Funding
- National Institutes of Health [T32 HLO7572, P30-HD18655]
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Granulocytes generate a respiratory burst'' of NADPH oxidase-dependent superoxide anion (O-2(-center dot)) production that is required for efficient clearance of bacterial pathogens. Hv1 mediates a voltage-gated H+ channel activity that is proposed to serve a charge-balancing role in granulocytic phagocytes such as neutrophils and eosinophils. Using mice in which the gene encoding Hv1 is replaced by beta-Geo reporter protein sequence, we show that Hv1 expression is required for measurable voltage-gated H+ current in unstimulated phagocytes. O-2(-center dot) production is substantially reduced in the absence of Hv1, suggesting that Hv1 contributes a majority of the charge compensation required for optimal NADPH oxidase activity. Despite significant reduction in superoxide production, Hv1(-/-) mice are able to clear several types of bacterial infections.
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