Cited by 109Heme Oxygenase-1 and Carbon MonoxideNitric Oxide and Endothelin EffectsSulfur Compounds in Biology

Gaseous mediators in resolution of inflammation

Wallace, John L., Ianaro, Angela, Flannigan, Kyle L., Cirino, Giuseppe·2015·Seminars in Immunology

Abstract

There are numerous gaseous substances that can act as signaling molecules, but the best characterized of these are nitric oxide, hydrogen sulfide and carbon monoxide. Each has been shown to play important roles in many physiological and pathophysiological processes. This article is focused on the effects of these gasotransmitters in the context of inflammation. There is considerable overlap in the actions of nitric oxide, hydrogen sulfide and carbon monoxide with respect to inflammation, and these mediators appear to act primarily as anti-inflammatory substances, promoting resolution of inflammatory processes. They also have protective and pro-healing effects in some tissues, such as the gastrointestinal tract and lung. Over the past two decades, significant progress has been made in the development of novel anti-inflammatory and cytoprotective drugs that release of one or more of these gaseous mediators.

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Crossref · 10.1016/j.smim.2015.05.004

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  • Excess NO during inflammation may induce apoptosis of proinflammatory immune cells, which are then cleared by immune-suppressive macrophages, indicating high NO level as a mediator of pro-resolving process.

    “But it was also suggested that excess NO during inflammation may induce the apoptosis of proinflammatory immune cells which was then cleared by immune-suppressive macrophage, indicating high NO level as a mediator of pro-resolving process.449”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [449]

  • CO may contribute to HO1's anti-inflammatory effects by restricting leukocyte entry into inflamed sites and reducing cytokine release.

    “CO might contribute to the anti-inflammatory functions of HO1 by limiting leukocyte infiltration into inflammatory sites and suppressing cytokine production130.”

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References 108 · Cited by 109

Authors
Wallace, J. L., Ianaro, A., Flannigan, K. L., & Cirino, G.
Affiliations
  • University of Calgary (CA)
  • University of Naples Federico II (IT)
  • Georgia State University (US)
Corresponding author
Wallace, John L.
Venue
Seminars in Immunology
Publisher
Elsevier BV
Published
2015-05
Volume
27
Issue
3
Pages
227-233
ISSN
1044-5323 (ISSN-L)
OpenAlex
W616853799
Cited by
109
References
108
Citations by year
2026: 4 · 2025: 4 · 2024: 7 · 2023: 10 · 2022: 11 · 2021: 11 · 2020: 11 · 2019: 13 · 2018: 7 · 2017: 17 · 2016: 11 · 2015: 3
FWCI
1.23
Type
journal article
Language
en
Open access
closed
Locations
  • Seminars in Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heme Oxygenase-1 and Carbon Monoxide
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
Keywords
gasotransmitters, nitric oxide, hydrogen sulfide, carbon monoxide, inflammation resolution, anti-inflammatory signaling, cytoprotection, gastrointestinal inflammation, lung inflammation, drug development
MeSH terms
Anti-Inflammatory Agents, Carbon Monoxide, Homeostasis, Humans, Hydrogen Sulfide, Inflammation, Nitric Oxide, Signal Transduction, Apoptosis, Cytoprotection, Gasotransmitters

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