Nrf2 suppresses macrophage inflammatory response by blocking proinflammatory cytokine transcription
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Nrf2 (NF-E2-related factor-2) transcription factor regulates oxidative/xenobiotic stress response and also represses inflammation. However, the mechanisms how Nrf2 alleviates inflammation are still unclear. Here, we demonstrate that Nrf2 interferes with lipopolysaccharide-induced transcriptional upregulation of proinflammatory cytokines, including IL-6 and IL-1β. Chromatin immunoprecipitation (ChIP)-seq and ChIP-qPCR analyses revealed that Nrf2 binds to the proximity of these genes in macrophages and inhibits RNA Pol II recruitment. Further, we found that Nrf2-mediated inhibition is independent of the Nrf2-binding motif and reactive oxygen species level. Murine inflammatory models further demonstrated that Nrf2 interferes with IL6 induction and inflammatory phenotypes in vivo . Thus, contrary to the widely accepted view that Nrf2 suppresses inflammation through redox control, we demonstrate here that Nrf2 opposes transcriptional upregulation of proinflammatory cytokine genes. This study identifies Nrf2 as the upstream regulator of cytokine production and establishes a molecular basis for an Nrf2-mediated anti-inflammation approach.
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Nrf2's role in inflammation is not limited to just oxidative stress control.
“suggesting that Nrf2’s role in inflammation is not limited to just oxidative stress control [198].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [198]
Nrf2 blocks the transcriptional upregulation of pro-inflammatory cytokine genes including IL-6 and IL-1β in an ARE-independent manner through direct binding to the proximity of pro-inflammatory genes to inhibit RNA polymerase II recruitment.
“Nrf2 has also been found to block the transcriptional upregulation of pro-inflammatory cytokine genes including interleukin 6 (IL-6) and interleukin 1 beta (IL-1β) in an ARE-independent manner through direct binding to the proximity of pro-inflammatory genes to inhibit RNA polymerase II recruitment”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [198]
Expression of pro-inflammatory cytokine genes in M1 macrophages is inhibited by Nrf2-ARE binding.
“the expression of pro-inflammatory cytokine genes in M1 macrophages is inhibited by Nrf2-ARE binding [198]”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [198]
IRG1 plays a major role in embryo implantation in the womb.
“it also appears to play a major role in embryo implantation in the womb, a process thought to require immunosuppression70–72.”
From Coupling Krebs cycle metabolites to signalling in immunity and cancer (2018) · cites this paper as [72]
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- Authors
- Kobayashi, E. H., Suzuki, T., Funayama, R., Nagashima, T., Hayashi, M., Sekine, H., Tanaka, N., Moriguchi, T., Motohashi, H., Nakayama, K., & Yamamoto, M.
- Affiliations
- Tohoku University (JP)
- Miyagi Prefectural Hospital Organization (JP)
- Institute of Development, Aging and Cancer, Tohoku University (JP)
- Corresponding author
- Kobayashi, Eri H.
- Yamamoto, Masayuki
- ORCID
- Venue
- Nature Communications
- Published
- 2016-05-23
- Volume
- 7
- Issue
- 1
- Pages
- 11624-11624
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4879264
- OpenAlex
- W2400239628
- Cited by
- 1,878
- References
- 58
- Citations by year
- 2026: 188 · 2025: 244 · 2024: 245 · 2023: 214 · 2022: 243 · 2021: 209 · 2020: 236 · 2019: 115 · 2018: 109 · 2017: 61 · 2016: 13
- FWCI
- 51.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- The Japanese Biochemical Society
- Funders
- Japan Agency for Medical Research and Development (CREST)
- Ministry of Education, Culture, Sports, Science and Technology (23116002, 22118002, 24249015, CREST)
- Japan Society for the Promotion of Science (15K14414, 15H04692, 16H05147, 26111002, 24249015, 25840001, CREST, 15K08257, 16K15228)
- Core Research for Evolutional Science and Technology
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- Nrf2, macrophages, inflammation, inflammatory cytokines, interleukin-6, IL-1β, transcriptional repression, RNA polymerase II recruitment, lipopolysaccharide, anti-inflammatory mechanism, oxidative stress response
- MeSH terms
- Animals, Gene Expression Regulation, Inflammation, Macrophages, Mice, Inbred C57BL, Mice, Inbred ICR, RNA Polymerase II, Cytokines, Mice, Knockout, Oxidative Stress, NF-E2-Related Factor 2
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