ArticleFrontiers in immunology2019
Exclusive Temporal Stimulation of IL-10 Expression in LPS-Stimulated Mouse Macrophages by cAMP Inducers and Type I Interferons.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
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- Tenofovir, Interferon Pathways, and Mucosal Immunity: Implications for People Living With HIV.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Review
- The Dual Role of Interleukin-10 in Sepsis: Research Progress and Therapeutic Prospects.Inflammation · 2026Review
- Comparative renoprotective effects of phoenixin-14, a novel peptide, and dexamethasone in LPS-induced sepsis: targeting inflammation, oxidative stress, and apoptosis.Apoptosis : an international journal on programmed cell death · 2026Article
- Integrated transcriptomic and functional analyses reveal that NOX2 inhibition rewires the inflammatory landscape of macrophages.Frontiers in immunology · 2026Article
- Microglial Histaminergic Signaling Promotes Interleukin-10 Production and Ameliorates Motor Dysfunction in Parkinson's Disease.Aging and disease · 2025Article
- Lipid Nanoparticles With Fine-Tuned Composition Show Enhanced Colon Targeting as a Platform for mRNA Therapeutics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Revisiting the Immunometabolic Basis for the Metabolic Syndrome from an Immunonutritional View.Biomedicines · 2024Review
- Treatment with β-Adrenoceptor Agonist Isoproterenol Reduces Non-parenchymal Cell Responses in LPS/D-GalN-Induced Liver Injury.Inflammation · 2024Article
- cAMP-PKA/EPAC signaling and cancer: the interplay in tumor microenvironment.Journal of hematology & oncology · 2024Review
- Type I Interferon, Induced by Adenovirus or Adenoviral Vector Infection, Regulates the Cytokine Response to Lipopolysaccharide in a Macrophage Type-Specific Manner.Journal of innate immunity · 2024Article
- Nanoparticles containing intracellular proteins modulate neutrophil functional and phenotypic heterogeneity.Frontiers in immunology · 2024Article
- Investigation of Correlation between Resistance to Diazepam and Expression of Inflammatory Markers in The Peripheral Blood of Patients with Status Epilepticus.Acta medica academica · 2023Article
- Total Lipid Extracts of Honeybee Drone Larvae Are Modulated by Extraction Temperature and Display Consistent Anti-Inflammatory Potential.Foods (Basel, Switzerland) · 2023Article
- New insights into the suppression of inflammation and lipid accumulation byGenes & diseases · 2023Review
- Inhibitory effects ofHeliyon · 2023Article
- TLR4 activation by lysozyme induces pain without inflammation.Frontiers in immunology · 2023Article
- Single-cell analysis reveals TLR-induced macrophage heterogeneity and quorum sensing dictate population wide anti-inflammatory feedback in response to LPS.Frontiers in immunology · 2023Article
- Regulation of mRNA stability contributes to the function of innate lymphoid cells in various diseases.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the key anti-inflammatory cytokine IL-10 in lipopolysaccharide (LPS)-stimulated macrophages is mediated by a delayed autocrine/paracrine loop of type I interferons (IFN) to ensure timely attenuation of inflammation. We have previously shown that cAMP synergizes with early IL-10 expression by LPS, but is unable to amplify the late type I IFN-dependent activity. We now examined the mechanism of this synergistic transcription in mouse macrophages at the promoter level, and explored the crosstalk between type I IFN signaling and cAMP, using the β-adrenergic receptor agonist, isoproterenol, as a cAMP inducer. We show that silencing of the type I IFN receptor enables isoproterenol to synergize with LPS also at the late phase, implying that autocrine type I IFN activity hinders synergistic augmentation of LPS-stimulated IL-10 expression by cAMP at the late phase. Furthermore, IL-10 expression in LPS-stimulated macrophages is exclusively stimulated by either IFNα or isoproterenol. We identified a set of two proximate and inter-dependent cAMP response element (CRE) sites that cooperatively regulate early IL-10 transcription in response to isoproterenol-stimulated CREB and that further synergize with a constitutive Sp1 site. At the late phase, up-regulation of Sp1 activity by LPS-stimulated type I IFN is correlated with loss of function of the CRE sites, suggesting a mechanism for the loss of synergism when LPS-stimulated macrophages switch to type I IFN-dependent IL-10 expression. This report delineates the molecular mechanism of cAMP-accelerated IL-10 transcription in LPS-stimulated murine macrophages that can limit inflammation at its onset.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.