ArticleAmerican journal of respiratory cell and molecular biology2012
Cooperation between classical and alternative NF-κB pathways regulates proinflammatory responses in epithelial cells.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Defining the Critical Role of α-Gustducin for NF-κB Inhibition and Anti-Inflammatory Signal Transduction by Bitter Agonists in Lung Epithelium.International journal of molecular sciences · 2026Article
- Nanotechnology-Based Drug Delivery Approaches of Mangiferin: Promises, Reality and Challenges in Cancer Chemotherapy.Cancers · 2023Review
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- Transcriptomic modifications in developmental cardiopulmonary adaptations to chronic hypoxia using a murine model of simulated high-altitude exposure.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Dysregulation of the glutaredoxin/American journal of physiology. Cell physiology · 2020Article
- A detrimental role of RelB in mature oligodendrocytes during experimental acute encephalomyelitis.Journal of neuroinflammation · 2019Article
- 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
- p52 expression enhances lung cancer progression.Scientific reports · 2018Article
- Inhaled Cryptococcus neoformans elicits allergic airway inflammation independent of Nuclear Factor Kappa B signalling in lung epithelial cells.Immunology · 2018Article
- NR4A Receptors Differentially Regulate NF-κB Signaling in Myeloid Cells.Frontiers in immunology · 2017Article
- Glutathione S-transferase pi modulates NF-κB activation and pro-inflammatory responses in lung epithelial cells.Redox biology · 2016Article
- Mangiferin and Cancer: Mechanisms of Action.Nutrients · 2016Review
- p52 Overexpression Increases Epithelial Apoptosis, Enhances Lung Injury, and Reduces Survival after Lipopolysaccharide Treatment.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Club Cell-16 and RelB as Novel Determinants of Arterial Stiffness in Exacerbating COPD Patients.PloS one · 2016Article
- Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells.Human molecular genetics · 2015Article
- The glutaredoxin/S-glutathionylation axis regulates interleukin-17A-induced proinflammatory responses in lung epithelial cells in association with S-glutathionylation of nuclear factor κB family proteins.Free radical biology & medicine · 2014Article
- An anti-leishmanial thiadiazine agent induces multiple myeloma cell apoptosis by suppressing the nuclear factor kappaB signalling pathway.British journal of cancer · 2014Article
- Article
- Epithelial NF-κB orchestrates house dust mite-induced airway inflammation, hyperresponsiveness, and fibrotic remodeling.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- RelB: an outlier in leukocyte biology.Journal of leukocyte biology · 2013Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor NF-κB has been causally linked to inflammatory lung diseases. Recent studies have unraveled the complexity of NF-κB activation by identifying two parallel activation pathways: the classical NF-κB pathway, which is controlled by IκB kinase complex-β (IKKβ) and RelA/p50, and the alternative pathway, which is controlled by IKKα and RelB/p52. The alternative pathway regulates adaptive immune responses and lymphoid development, yet its role in the regulation of innate immune responses remains largely unknown. In this study, we determined the relevance of the alternative NF-κB pathway in proinflammatory responses in lung epithelial cells. The exposure of C10 murine alveolar lung epithelial cells to diverse stimuli, or primary murine tracheal epithelial cells to LPS, resulted in the activation of both NF-κB pathways, based on the nuclear translocation of RelA, p50, RelB, and p52. Increases in the nuclear content of RelA occurred rapidly, but transiently, whereas increases in nuclear RelB content were protracted. The small interfering (si) RNA-mediated knockdown of IKKα, RelA, or RelB resulted in decreases of multiple LPS-induced proinflammatory cytokines. Surprisingly, the siRNA ablation of IKKα or RelB led to marked increases in the production of IL-6 in response to LPS. The simultaneous expression of constitutively active (CA)-IKKα and CA-IKKβ caused synergistic increases in proinflammatory mediators. Lastly, the disruption of the IKK signalsome inhibited the activation of both NF-κB pathways. These results demonstrate that the coordinated activation of both NF-κB pathways regulates the magnitude and nature of proinflammatory responses in lung epithelial cells.
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