Cited by 892Redox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative MechanismsNitric Oxide and Endothelin Effects

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Reactive Oxygen Species and Cell Signaling: Respiratory Burst in Macrophage Signaling

Forman, Henry Jay, Torres, Martine·2002·American Journal of Respiratory and Critical Care Medicine

DOI 10.1164/rccm.2206007

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Abstract

Phagocytes such as neutrophils and macrophages produce reactive oxygen species (ROS) during phagocytosis or stimulation with a wide variety of agents through activation of nicotinamide adenine dinucleotide phosphate reduced (NADPH) oxidase that is assembled at the plasma membrane from resident plasma membrane and cytosolic protein components. One of the subunits of the phagocyte NADPH oxidase is now recognized as a member of a family of NADPH oxidases, or NOX, present in cells other than phagocytes. Physiologic generation of ROS has been implicated in a variety of physiologic responses from transcriptional activation to cell proliferation and apoptosis. The increase in superoxide and hydrogen peroxide (H2O2) that results from stimulation of the NADPH oxidase is transient, in part due to the presence of the antioxidant enzymes, which return their concentrations to the prestimulation steady state level. Thus, the antioxidant enzymes may function in the “turn-off” phase of signal transduction by ROS. During its transient elevation, H2O2 may act as a modifier of key signaling enzymes through reversible oxidation of critical thiols. The rapid reaction of thiols with H2O2 when in their unprotonated state would provide a potential mechanism for the specificity that is necessary for physiologic cell signaling.

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Authors: Forman, H. J., & Torres, M.
Affiliations: University of Southern California (US)
Department of Environmental Health Sciences, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama; and Department of Pediatrics, Children's Hospital Los Angeles Research Institute, Keck School of Medicine, University of Southern California, Los Angeles, California
ORCID: Forman, Henry Jay
Venue: American Journal of Respiratory and Critical Care Medicine
Publisher: Oxford University Press (OUP)
Published: 2002-12
Volume: 166
Issue: Supplement_1
Pages: S4-S8
ISSN: 1073-449X (ISSN-L)
1535-4970
DOI: 10.1164/rccm.2206007
OpenAlex: W1874751834
Cited by: 891
References: 67
Citations by year: 2026: 18 · 2025: 21 · 2024: 23 · 2023: 32 · 2022: 47 · 2021: 44 · 2020: 36 · 2019: 31 · 2018: 44 · 2017: 43 · 2016: 50 · 2015: 43 · 2014: 48 · 2013: 45 · 2012: 44
FWCI: 2.28
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: American Journal of Respiratory and Critical Care Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (R01HL037556, HL 37556)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords: reactive oxygen species, NADPH oxidase, respiratory burst, macrophages, signal transduction, hydrogen peroxide, superoxide, antioxidant enzymes, thioredoxin reductase, thioredoxin, redox signaling, phagocytes
MeSH terms: Humans, Hydrogen Peroxide, Macrophages, Oxidation-Reduction, Signal Transduction, Respiratory Burst, Protein Tyrosine Phosphatases, Reactive Oxygen Species, Mitogen-Activated Protein Kinases

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Reactive Oxygen Species and Cell Signaling: Respiratory Burst in Macrophage Signaling

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