The regulatory role of nitric oxide in proinflammatory cytokine expression during the induction and resolution of inflammation
Abstract
Nitric oxide is produced in various settings, including encounters with apoptotic cells, for regulation of cytokine expression, thereby contributing to inflammation. Upon inflammation, neutrophils and subsequently monocytes infiltrate into the involved site. Neutrophils perform functions such as bacterial killing or tissue destruction and then undergo apoptosis, whereas monocytes differentiate into macrophages at the site. Macrophages and other phagocytes finally clear apoptotic neutrophils, leading to resolution of the inflammation. One of the key steps during inflammation is leukocyte infiltration, which is controlled chiefly by chemokines for neutrophils and monocytes. The production of these chemokines is regulated positively or negatively by iNOS-derived NO. Although the mechanisms underlying such dual effects of NO remain unknown, the level of NO and duration of NO exposure appear to be determining factors. The clearance of apoptotic neutrophils without causing further proinflammatory responses, on the other hand, is another key event during inflammation. The production of proinflammatory cytokines appears to be actively suppressed by TGF-β and NO, which are produced by phagocytes upon interaction with apoptotic cells. Overall, NO plays a critical role during inflammation and therefore, remains a potential target for developing therapeutics for inflammatory diseases.
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•NO plays an important role during inflammation and is a potential target for therapeutic development in inflammatory diseases.
“In summary, •NO plays an important role during inflammation and is a potential target for therapeutic development in inflammatory diseases [124].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [124]
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- Authors
- Kobayashi, Y.
- Affiliations
- Toho University (JP)
- Corresponding author
- Kobayashi, Yoshiro
- ORCID
- Kobayashi, Yoshiro
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-08-31
- Volume
- 88
- Issue
- 6
- Pages
- 1157-1162
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- OpenAlex
- W2116137306
- Cited by
- 306
- References
- 46
- Citations by year
- 2026: 11 · 2025: 19 · 2024: 18 · 2023: 23 · 2022: 22 · 2021: 21 · 2020: 18 · 2019: 27 · 2018: 15 · 2017: 15 · 2016: 19 · 2015: 27 · 2014: 22 · 2013: 21 · 2012: 21
- FWCI
- 1.25
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- nitric oxide, inflammatory cytokines, inflammation resolution, neutrophil apoptosis, monocyte differentiation, macrophages, chemokines, leukocyte infiltration, inducible nitric oxide synthase, TGF-beta, efferocytosis, phagocytes, inflammatory diseases
- MeSH terms
- Animals, Dendritic Cells, Humans, Inflammation, Nitric Oxide, Cytokines, NF-kappa B, S-Nitroso-N-Acetylpenicillamine, Mice, Nitric Oxide Synthase Type II
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