ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
cAMP-dependent protein kinase activation decreases cytokine release in bronchial epithelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Metastasis-Associated Wound Repair Promotes Reciprocal Lung Epithelium Activation and Breast Cancer Metastatic Outgrowth.Cancer research communications · 2026Article
- 8-Bromo-cAMP attenuates human airway epithelial barrier disruption caused by titanium dioxide fine and nanoparticles.Tissue barriers · 2024Article
- Zinc Protects against Swine Barn Dust-Induced Cilia Slowing.Biomolecules · 2024Article
- Effect of epithelial-specific MyD88 signaling pathway on airway inflammatory response to organic dust exposure.Journal of immunotoxicology · 2023Article
- Fusion of the βFASEB bioAdvances · 2022Article
- Inhibition of phosphodiesterase-4 in the spinal dorsal horn ameliorates neuropathic pain via cAMP-cytokine-Cx43 signaling in mice.CNS neuroscience & therapeutics · 2022Article
- Increased Retinal Ganglion Cell Survival by Exogenous IL-2 Depends on IL-10, Dopamine D1 Receptors, and Classical IL-2/IL-2R Signaling Pathways.Neurochemical research · 2021Article
- Article
- Clinical Relevance of the Anti-inflammatory Effects of Roflumilast on Human Bronchus: Potentiation by a Long-Acting Beta-2-Agonist.Frontiers in pharmacology · 2020Article
- Challenge model of TNFJournal of pharmacokinetics and pharmacodynamics · 2019Article
- Ethyl pyruvate reduces organic dust-induced airway inflammation by targeting HMGB1-RAGE signaling.Respiratory research · 2019Article
- MyD88 controls airway epithelial Muc5ac expression during TLR activation conditions from agricultural organic dust exposure.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Thrombin-cleaved syndecan-3/-4 ectodomain fragments mediate endothelial barrier dysfunction.PloS one · 2019Article
- Kinome analyses of inflammatory responses to swine barn dust extract in human bronchial epithelial and monocyte cell lines.Innate immunity · 2018Article
- Docosahexaenoic acid enhances amphiregulin-mediated bronchial epithelial cell repair processes following organic dust exposure.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Epac Function and cAMP Scaffolds in the Heart and Lung.Journal of cardiovascular development and disease · 2018Review
- Dimethylarginine dimethylaminohydrolase (DDAH) overexpression enhances wound repair in airway epithelial cells exposed to agricultural organic dust.Inhalation toxicology · 2018Article
- Alcohol Inhibits Organic Dust-induced ICAM-1 Expression on Bronchial Epithelial Cells.Safety (Basel, Switzerland) · 2017Article
- β2-Adrenergic agonists attenuate organic dust-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Alcohol Decreases Organic Dust-Stimulated Airway Epithelial TNF-Alpha Through a Nitric Oxide and Protein Kinase-Mediated Inhibition of TACE.Alcoholism, clinical and experimental research · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Lung injury caused by inhalation of dust from swine-concentrated animal-feeding operations (CAFO) involves the release of inflammatory cytokine interleukin 8 (IL-8), which is mediated by protein kinase C-ε (PKC-ε) in airway epithelial cells. Once activated by CAFO dust, PKC-ε is responsible for slowing cilia beating and reducing cell migration for wound repair. Conversely, the cAMP-dependent protein kinase (PKA) stimulates contrasting effects, such as increased cilia beating and an acceleration of cell migration for wound repair. We hypothesized that a bidirectional mechanism involving PKA and PKC regulates epithelial airway inflammatory responses. To test this hypothesis, primary human bronchial epithelial cells and BEAS-2B cells were treated with hog dust extract (HDE) in the presence or absence of cAMP. PKC-ε activity was significantly reduced in cells that were pretreated for 1 h with 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) before exposure to HDE (P < 0.05). HDE-induced IL-6, and IL-8 release was significantly lower in cells that were pretreated with 8-Br-cAMP (P < 0.05). To exclude exchange protein activated by cAMP (EPAC) involvement, cells were pretreated with either 8-Br-cAMP or 8-(4-chlorophenylthio)-2'-O-methyladenosine-3',5'-cyclic monophosphate (8-CPT-2Me-cAMP) (EPAC agonist). 8-CPT-2Me-cAMP did not activate PKA and did not reduce HDE-stimulated IL-6 release. In contrast, 8-Br-cAMP decreased HDE-stimulated tumor necrosis factor (TNF)-α-converting enzyme (TACE; ADAM-17) activity and subsequent TNF-α release (P < 0.001). 8-Br-cAMP also blocked HDE-stimulated IL-6 and keratinocyte-derived chemokine release in precision-cut mouse lung slices (P < 0.05). These data show bidirectional regulation of PKC-ε via a PKA-mediated inhibition of TACE activity resulting in reduced PKC-ε-mediated release of IL-6 and IL-8.
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Registered trials
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