ArticleAmerican journal of respiratory and critical care medicine2008
Nuclear factor-kappaB activation in airway epithelium induces inflammation and hyperresponsiveness.
Article in American journal of respiratory and critical care medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 121 citations in OpenAlex.
- Oxidative stress driven airway mesenchymal reprogramming in asthma: mechanistic insights and evidence from botanical drug formulations.Frontiers in pharmacology · 2026Review
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- Effects of a Peptide Derived from the Primary Sequence of a Kallikrein Inhibitor Isolated fromInternational journal of molecular sciences · 2023Article
- Modulating asthma-COPD overlap responses with IL-17 inhibition.Frontiers in immunology · 2023Article
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- Airway remodeling: TheFrontiers in allergy · 2022Review
- Vitamin D Supplementation: Oxidative Stress Modulation in a Mouse Model of Ovalbumin-Induced Acute Asthmatic Airway Inflammation.International journal of molecular sciences · 2021Article
- E-Cadherin: An Important Functional Molecule at Respiratory Barrier Between Defence and Dysfunction.Frontiers in physiology · 2021Review
- Nuclear factor kappa B activation in cardiomyocytes by serum of children with obstructive sleep apnea syndrome.Scientific reports · 2020Article
- Glutaredoxin deficiency promotes activation of the transforming growth factor beta pathway in airway epithelial cells, in association with fibrotic airway remodeling.Redox biology · 2020Article
- Spilanthol Inhibits COX-2 and ICAM-1 Expression via Suppression of NF-κB and MAPK Signaling in Interleukin-1β-Stimulated Human Lung Epithelial Cells.Inflammation · 2018Article
- Long-term endurance running activity causes pulmonary changes depending on the receptor for advanced glycation end-products.Pflugers Archiv : European journal of physiology · 2018Article
- IL-1/inhibitory κB kinase ε-induced glycolysis augment epithelial effector function and promote allergic airways disease.The Journal of allergy and clinical immunology · 2018Article
- Effect of Anti-IL17 Antibody Treatment Alone and in Combination With Rho-Kinase Inhibitor in a Murine Model of Asthma.Frontiers in physiology · 2018Article
- The Plant Proteinase InhibitorBioMed research international · 2018Article
- Airway remodeling in asthma: what really matters.Cell and tissue research · 2017Review
- Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma.JCI insight · 2017Article
- Effects of Anti-IL-17 on Inflammation, Remodeling, and Oxidative Stress in an Experimental Model of Asthma Exacerbated by LPS.Frontiers in immunology · 2017Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
rationaleNuclear factor (NF)-kappaB is a prominent proinflammatory transcription factor that plays a critical role in allergic airway disease. Previous studies demonstrated that inhibition of NF-kappaB in airway epithelium causes attenuation of allergic inflammation.
objectivesWe sought to determine if selective activation of NF-kappaB within the airway epithelium in the absence of other agonists is sufficient to cause allergic airway disease.
methodsA transgenic mouse expressing a doxycycline (Dox)-inducible, constitutively active (CA) version of inhibitor of kappaB (IkappaB) kinase-beta (IKKbeta) under transcriptional control of the rat CC10 promoter, was generated. MEASUREMENTS AND MAIN
resultsAfter administration of Dox, expression of the CA-IKKbeta transgene induced the nuclear translocation of RelA in airway epithelium. IKKbeta-triggered activation of NF-kappaB led to an increased content of neutrophils and lymphocytes, and concomitant production of proinflammatory mediators, responses that were not observed in transgenic mice not receiving Dox, or in transgene-negative littermate control animals fed Dox. Unexpectedly, expression of the IKKbeta transgene in airway epithelium was sufficient to cause airway hyperresponsiveness and smooth muscle thickening in absence of an antigen sensitization and challenge regimen, the presence of eosinophils, or the induction of mucus metaplasia.
conclusionsThese findings demonstrate that selective activation NF-kappaB in airway epithelium is sufficient to induce airway hyperresponsiveness and smooth muscle thickening, which are both critical features of allergic airway disease.
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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.