Using ROS as a Second Messenger, NADPH Oxidase 2 Mediates Macrophage Senescence via Interaction with NF‐ κ B during Pseudomonas aeruginosa Infection
Open accessAbstract
Pseudomonas aeruginosa (PA) is one of the most prevalent pathogens that cause nosocomial infection in critical patients. However, the mechanisms underlying macrophage growth status and functional changes during PA infection are yet unknown. In the present study, NADPH oxidase, gp91 phox (NOX2) mediated macrophage to senescence in a PAO1 colony‐dependent manner. gp91 phox might regulate the senescence process through mutual interaction with the NF‐ κ B pathway. During infection, the overexpression or downregulation of gp91 phox in macrophage could affect the nuclear activity of NF‐ κ B p65, while the downregulation of NF‐ κ B p65 led to a suppressed expression of gp91 phox . Reactive oxygen species (ROS) served as the second messenger between both molecules as the ROS inhibitor, N ‐acetylcysteine (NAC), could partially restore these changes. Consequently, the level of ROS and inflammatory cytokines, including IL‐6 and TNF α , elevated during PAO1 infection, and their production altered as a result of the genetic manipulation of gp91 phox and NF‐ κ B p65, as well as NAC treatment. Also, the senescent phenotypes, SA‐ β ‐gal staining and p16 ink4a , changed after genetic manipulation with gp91 phox and NF‐ κ B p65 and NAC treatment. The capacity of phagocytosis in macrophages was decreased during senescence. In conclusion, PA directs the macrophage towards senescence, and senescent macrophages exhibit a decreased ability of phagocytosis. This process of senescence was regulated by the interactions between NADPH oxidase gp91 phox and NF‐ κ B p65 via ROS as a second messenger.
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Overexpression of gp91phox increased NFκB activation.
“Whilst overexpression of gp91phox increased NFκB activation.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [147]
NFκB may reciprocally regulate NOX2 expression, since its downregulation suppresses gp91phox in the same model.
“Further, NFκB may reciprocally regulate NOX2 expression, since its downregulation suppresses gp91phox in the same model.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [147]
Oxidative stress and inflammation are undoubtedly linked.
“The two are undoubtedly linked; however, it is not clear how ROS interact with glia to elicit an immune response, although this may involve reciprocal regulation between NOX2 and NFκB [147].”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [147]
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- Authors
- Li, H., Luo, Y.-F., Wang, Y.-S., Yang, Q., Xiao, Y.-L., Cai, H.-R., & Xie, C.-M.
- Affiliations
- Nanjing Drum Tower Hospital (CN)
- Second Affiliated Hospital of Nanchang University (CN)
- The First Affiliated Hospital, Sun Yat-sen University (CN)
- Corresponding author
- Li, Hui
- Xie, Can-Mao
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2018-01
- Volume
- 2018
- Issue
- 1
- Pages
- 9741838-9741838
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC6040290
- OpenAlex
- W2811325457
- Cited by
- 45
- References
- 34
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 6 · 2023: 5 · 2022: 7 · 2021: 7 · 2020: 4 · 2019: 4
- FWCI
- 1.33
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Fundamental Research Funds for the Central Universities (20620140669, 81400011)
- National Natural Science Fund of China (20620140669, 81400011)
- 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 › Telomeres, Telomerase, and Senescence
- Keywords
- macrophage senescence, NADPH oxidase 2, gp91phox, NF-κB p65, reactive oxygen species, second messengers, Pseudomonas aeruginosa infection, N-acetylcysteine, phagocytosis, p16INK4a, interleukin-6, TNF-α
- MeSH terms
- NADPH Oxidase 2, Acetylcysteine, Animals, Humans, Macrophages, Pseudomonas aeruginosa, Pseudomonas Infections, Tumor Necrosis Factor-alpha, Interleukin-6, NF-kappa B, Cellular Senescence, Reactive Oxygen Species
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