Cited by 1,676Neutrophil, Myeloperoxidase and Oxidative MechanismsRedox biology and oxidative stressNitric Oxide and Endothelin Effects

Antimicrobial reactive oxygen and nitrogen species: concepts and controversies

Fang, Ferric C.·2004·Nature Reviews Microbiology

Abstract

Phagocyte-derived reactive oxygen and nitrogen species are of crucial importance for host resistance to microbial pathogens. Decades of research have provided a detailed understanding of the regulation, generation and actions of these molecular mediators, as well as their roles in resisting infection. However, differences of opinion remain with regard to their host specificity, cell biology, sources and interactions with one another or with myeloperoxidase and granule proteases. More than a century after Metchnikoff first described phagocytosis, and more than four decades after the discovery of the burst of oxygen consumption that is associated with microbial killing, the seemingly elementary question of how phagocytes inhibit, kill and degrade microorganisms remains controversial. This review updates the reader on these concepts and the topical questions in the field.

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Crossref · 10.1038/nrmicro1004

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244 of 244 references verified0 citation errors · 0 not checkable

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  • After crossing the phagosomal membrane, NO and ROI can spontaneously react in the phagosomal lumen to generate nitrogen dioxide, peroxynitrite, dinitrogen trioxide, nitrosothiols, nitroxyl, and dinitrosyl-iron complexes.

    “After crossing the phagosomal membrane, NO and ROI can spontaneously react in the phagosomal lumen to generate nitrogen dioxide (NO2), peroxynitrite (ONOO−), dinitrogen trioxide (N2O3), nitrosothiols, nitroxyl (HNO), and dinitrosyl-iron complexes (58).”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [58]

  • Activated macrophages produce reactive oxygen intermediates via activation of NOX2.

    “In parallel, activated macrophages produce reactive oxygen intermediates (ROI) via activation of NOX2 (58).”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [58]

  • Highly reactive intermediates execute their microbicidal activity by oxidative destruction of membrane lipids, DNA, thiol and tyrosine residues, whereas NO can exert toxicity by directly targeting iron sulfur clusters of central metabolic enzymes.

    “Nonetheless, these highly reactive intermediates execute their microbicidal activity by oxidative destruction of membrane lipids, DNA, thiol and tyrosine residues, whereas NO can exert toxicity by directly targeting iron sulfur cluster of central metabolic enzymes (57, 58, 70–72).”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [58]

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Authors
Fang, F. C.
Affiliations
University of Washington (US)
Corresponding author
Fang, Ferric C.
Venue
Nature Reviews Microbiology
Published
2004-10
Volume
2
Issue
10
Pages
820-832
ISSN
  • 1740-1526 (ISSN-L)
  • 1740-1534
OpenAlex
W2066515050
Cited by
1,676
References
245
Citations by year
2026: 56 · 2025: 73 · 2024: 81 · 2023: 72 · 2022: 89 · 2021: 129 · 2020: 104 · 2019: 113 · 2018: 83 · 2017: 88 · 2016: 110 · 2015: 70 · 2014: 93 · 2013: 79 · 2012: 90
FWCI
2.90
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Reviews Microbiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Fonds De La Recherche Scientifique - FNRS
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
reactive oxygen species, reactive nitrogen species, phagocytes, antimicrobial host defense, phagocytosis, myeloperoxidase, microbial killing, host specificity, respiratory burst
MeSH terms
Granulomatous Disease, Chronic, Humans, Immunity, Innate, Phagocytes, Polymorphism, Genetic, Cytokines, Reactive Oxygen Species, Nitric Oxide Synthase, Reactive Nitrogen Species, Nitric Oxide Synthase Type II

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