ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2005
Consequences of the electrogenic function of the phagocytic NADPH oxidase.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Molecular regulation of neutrophil swarming in health and disease: Lessons from the phagocyte oxidase.iScience · 2023Review
- Oxidative Stress and NADPH Oxidase: Connecting Electromagnetic Fields, Cation Channels and Biological Effects.International journal of molecular sciences · 2021Review
- Article
- Interactions between Neutrophils and Pseudomonas aeruginosa in Cystic Fibrosis.Pathogens (Basel, Switzerland) · 2017Review
- Dysregulated Ca2+ homeostasis in Fanconi anemia cells.Scientific reports · 2015Article
- Intracellular shunting of O2(-) contributes to charge compensation and preservation of neutrophil respiratory burst in the absence of voltage-gated proton channel activity.Experimental cell research · 2013Article
- Diverse novel functions of neutrophils in immunity, inflammation, and beyond.The Journal of experimental medicine · 2013Review
- Primary involvement of NADPH oxidase 4 in hypoxia-induced generation of reactive oxygen species in adipose-derived stem cells.Stem cells and development · 2012Article
- Neutrophils in innate host defense against Staphylococcus aureus infections.Seminars in immunopathology · 2012Review
- Small-molecule screen identifies reactive oxygen species as key regulators of neutrophil chemotaxis.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- VSOP/Hv1 proton channels sustain calcium entry, neutrophil migration, and superoxide production by limiting cell depolarization and acidification.The Journal of experimental medicine · 2010Article
- Hv1 proton channels are required for high-level NADPH oxidase-dependent superoxide production during the phagocyte respiratory burst.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- CLIC1 function is required for beta-amyloid-induced generation of reactive oxygen species by microglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Charge compensation for NADPH oxidase activity in microglia in rat brain slices does not involve a proton current.The European journal of neuroscience · 2008Article
- Role of Nox2 in elimination of microorganisms.Seminars in immunopathology · 2008Review
- The antibacterial activity of human neutrophils and eosinophils requires proton channels but not BK channels.The Journal of general physiology · 2006Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NADPH oxidase of phagocytic cells transfers a single electron from intracellular NADPH to extracellular O2, producing superoxide (O.-2), the precursor to several other reactive oxygen species. The finding that a genetic defect of the enzyme causes chronic granulomatous disease (CGD), characterized by recurrent severe bacterial infections, linked O.-2 generation to destruction of potentially pathogenic micro-organisms. In this review, we focus on the consequences of the electrogenic functioning of NADPH oxidase. We show that enzyme activity depends on the possibilities for compensating charge movements. In resting neutrophils K+ conductance dominates, but upon activation the plasma membrane rapidly depolarizes beyond the opening threshold of voltage-gated H+ channels and H+ efflux becomes the major charge compensating factor. K+ release is likely to contribute to the killing of certain bacteria but complete elimination only occurs if O.-2 production can proceed at full capacity. Finally, the reversed membrane potential of activated neutrophils inhibits Ca2+ entry, thereby preventing overloading the cells with Ca2+. Absence of this limiting mechanism in CGD cells may contribute to the pathogenesis of the disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.