ArticleBlood2015
NADPH oxidase controls neutrophilic response to sterile inflammation in mice by regulating the IL-1α/G-CSF axis.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Neutrophil NADPH oxidase breaks the inflammatory IL-1β/IL-17A circuit to enhance pathogen clearance during respiratory virus infections.Nature communications · 2026Article
- The Nox2 NADPH oxidase regulates neutrophilic inflammation in the oral cavity.Mucosal immunology · 2026Article
- Permissive lung neutrophils facilitate tuberculosis immunopathogenesis in male phagocyte NADPH oxidase-deficient mice.PLoS pathogens · 2024Article
- Immunoactivation by Cutaneous Blue Light Irradiation Inhibits Remote Tumor Growth and Metastasis.ACS pharmacology & translational science · 2024Article
- Modulation of Innate Immune Memory Dynamics by Subcellular Reactive Oxygen Species.Antioxidants & redox signaling · 2023Review
- NADPH oxidase 2 limits amplification of IL-1β-G-CSF axis and an immature neutrophil subset in murine lung inflammation.Blood advances · 2023Article
- IL-1/MyD88-Dependent G-CSF and IL-6 Secretion Mediates Postburn Anemia.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Detailed characterisation of invasive aspergillosis in a murine model of X-linked chronic granulomatous disease shows new insights in infections caused byFrontiers in cellular and infection microbiology · 2023Article
- Neutrophil and Macrophage NADPH Oxidase 2 Differentially Control Responses to Inflammation and to Aspergillus fumigatus in Mice.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Article
- NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology.Antioxidants (Basel, Switzerland) · 2021Review
- Pazopanib ameliorates acute lung injuries via inhibition of MAP3K2 and MAP3K3.Science translational medicine · 2021Article
- Blocking immunosuppressive neutrophils deters pY696-EZH2-driven brain metastases.Science translational medicine · 2020Article
- Article
- Dectin-1 Promotes Type I and III Interferon Expression to Support Optimal Antifungal Immunity in the Lung.Frontiers in cellular and infection microbiology · 2020Article
- Kawasaki disease and immunodeficiencies in children: case reports and literature review.Rheumatology international · 2019Review
- Metal Nanoparticles Released from Dental Implant Surfaces: Potential Contribution to Chronic Inflammation and Peri-Implant Bone Loss.Materials (Basel, Switzerland) · 2019Article
- Trauma Induces Emergency Hematopoiesis through IL-1/MyD88-Dependent Production of G-CSF.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- The roles of NADPH oxidase in modulating neutrophil effector responses.Molecular oral microbiology · 2019Review
- NADPH oxidase activation regulates apoptotic neutrophil clearance by murine macrophages.Blood · 2018Article
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9 authors at 2 institutions in 1 country.
Funding
Abstract
The leukocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase generates reactive oxygen species essential in microbial killing and regulation of inflammation. Inactivating mutations in this enzyme lead to chronic granulomatous disease (CGD), associated with increased susceptibility to both pyogenic infections and to inflammatory disorders. The role of the NADPH oxidase in regulating inflammation driven by nonmicrobial stimuli is poorly understood. Here, we show that NADPH oxidase deficiency enhances the early local release of interleukin-1α (IL-1α) in response to damaged cells, promoting an excessive granulocyte colony-stimulating factor (G-CSF)-regulated neutrophilic response and prolonged inflammation. In peritoneal inflammation elicited by tissue injury, X-linked Cybb-null (X-CGD) mice exhibited increased release of IL-1α and IL-1 receptor -mediated G-CSF production. In turn, higher levels of systemic G-CSF increased peripheral neutrophilia, which amplified neutrophilic peritoneal inflammation in X-CGD mice. Dampening early neutrophil recruitment by neutralization of IL-1α, G-CSF, or neutrophil depletion itself promoted resolution of otherwise prolonged inflammation in X-CGD. IL-1β played little role. Thus, we identified an excessive IL-1α/G-CSF response as a major driver of enhanced sterile inflammation in CGD in the response to damaged cells. More broadly, these results provide new insights into the regulation of sterile inflammation, and identify the NADPH oxidase in regulating the amplitude of the early neutrophilic response.
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Registered trials
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.