ArticleImmunology2010
The role of endothelial interleukin-8/NADPH oxidase 1 axis in sepsis.
Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Effects of the glucagon-like peptide-1 receptor agonist liraglutide on retinal endothelial function and oxidative stress during sepsis.Frontiers in pharmacology · 2026Article
- Article
- IL-8 (CXCL8) Correlations with Psychoneuroimmunological Processes and Neuropsychiatric Conditions.Journal of personalized medicine · 2024Review
- Endothelial cell metabolism in sepsis.World journal of emergency medicine · 2023Review
- Erythrocyte oxidative stress and thrombosis.Expert reviews in molecular medicine · 2022Review
- The Impact of Hypertension and Use of Calcium Channel Blockers on Tuberculosis Treatment Outcomes.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Article
- The association between interleukin-8 gene-251 A/T polymorphism and sepsis: A protocol for systematic review and meta analysis.Medicine · 2021Article
- Impaired capillary tube formation induced by elevated secretion of IL8 involves altered signaling via the CXCR1/PI3K/MMP2 pathway.Molecular biology reports · 2021Article
- Reactive Oxygen Species in Venous Thrombosis.International journal of molecular sciences · 2020Review
- IL-8 gene locus is associated with risk, severity and 28-day mortality of sepsis in a Chinese population.Clinical and experimental medicine · 2019Article
- Binding of EBP50 to Nox organizing subunit p47phox is pivotal to cellular reactive species generation and altered vascular phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- In Search of a Cure for Sepsis: Taming the Monster in Critical Care Medicine.Journal of innate immunity · 2016Review
- Lipopolysaccharide (LPS)-mediated angiopoietin-2-dependent autocrine angiogenesis is regulated by NADPH oxidase 2 (Nox2) in human pulmonary microvascular endothelial cells.The Journal of biological chemistry · 2015Article
- The ATP Receptors P2X7 and P2X4 Modulate High Glucose and Palmitate-Induced Inflammatory Responses in Endothelial Cells.PloS one · 2015Article
- Macrophage-specific NOX2 contributes to the development of lung emphysema through modulation of SIRT1/MMP-9 pathways.The Journal of pathology · 2015Article
- The pediatric sepsis biomarker risk model: potential implications for sepsis therapy and biology.Expert review of anti-infective therapy · 2014Review
- LPS-mediated endothelial activation in pulmonary endothelial cells: role of Nox2-dependent IKK-β phosphorylation.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- NOX enzymes: potential target for the treatment of acute lung injury.Cellular and molecular life sciences : CMLS · 2012Review
- Bench-to-bedside review: Neonatal sepsis-redox processes in pathogenesis.Critical care (London, England) · 2012Review
- Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Free radical biology & medicine · 2012Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a generalized inflammatory disease, caused by the hyperinflammatory response of the host, rather than by invading organisms. Endothelial cells play a crucial role in the pathogenesis of sepsis. In this study, we investigated the effects of interleukin-8 (IL-8), a known neutrophil chemoattractant, on lipopolysaccharide (LPS) -induced reactive oxygen species (ROS) production by endothelial cells, and its significance in the pathogenesis of LPS-mediated sepsis. The results revealed that IL-8 directly induced ROS production in human umbilical vein endothelial cells (HUVECs), and also mediated LPS-induced ROS production by HUVECs. Stimulation of HUVECs by LPS strongly enhanced tissue factor expression, a hallmark of severe sepsis, which was suppressed by IL-8 knockdown. We further discovered that NADPH oxidase (Nox) 1 expression in LPS-stimulated HUVECs was markedly repressed by IL-8 knockdown, and Nox1 knockdown reduced tissue factor expression, suggesting that the LPS/IL-8 signalling in endothelial cells was predominantly mediated by Nox1. In conclusion, LPS stimulation of endothelial cells causes activation of the IL-8-Nox1 axis, enhances the production of ROS, and ultimately contributes to the progression of severe sepsis.
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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.