ArticleBMC pulmonary medicine2020
Cigarette and IL-17A synergistically induce bronchial epithelial-mesenchymal transition via activating IL-17R/NF-κB signaling.
Article in BMC pulmonary medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Smoking and vaping alter genes related to mechanisms of SARS-CoV-2 susceptibility and severity: a systematic review and meta-analysis.The European respiratory journal · 2024Pooled it
- "The Ameliorative Effect of Interleukin-17A Neutralization on Doxorubicin-Induced Cardiotoxicity by Modulating the NF-κB/NLRP3/Caspase-1/IL-1β Signaling Pathway in Rats".Inflammation · 2025Article
- IL-17A regulates airway remodelling in COPD through the PI3K/AKT/mTOR pathway.Scientific reports · 2025Article
- Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.EXCLI journal · 2024Review
- NCR negative group 3 innate lymphoid cell (NCRImmunity, inflammation and disease · 2023Article
- Promotion of IL‑17/NF‑κB signaling in autoimmune thyroid diseases.Experimental and therapeutic medicine · 2023Article
- Cigarette Smoke Impairs Airway Epithelial Wound Repair: Role of Modulation of Epithelial-Mesenchymal Transition Processes and Notch-1 Signaling.Antioxidants (Basel, Switzerland) · 2022Article
- The effects of epithelial-mesenchymal transitions in COPD induced by cigarette smoke: an update.Respiratory research · 2022Review
- Function-specific IL-17A and dexamethasone interactions in primary human airway epithelial cells.Scientific reports · 2022Article
- Inhibition of NF-κB activation by BAY 11-7821 suppresses the proliferation and inflammation of glioma cells through inducing autophagy.Translational cancer research · 2022Article
- IL-17A Promotes Epithelial ADAM9 Expression in Cigarette Smoke-Related COPD.International journal of chronic obstructive pulmonary disease · 2022Article
- Role of Th17 Cytokines in Airway Remodeling in Asthma and Therapy Perspectives.Frontiers in allergy · 2022Review
- Pharmacological Rationale for Targeting IL-17 in Asthma.Frontiers in allergy · 2021Review
- Smoking Status Modifies the Relationship between Th2 Biomarkers and Small Airway Obstruction in Asthma.Canadian respiratory journal · 2021Article
- Relationships among smoking, oxidative stress, inflammation, macromolecular damage, and cancer.Mutation research. Reviews in mutation researchReview
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIL-17A directly induces epithelial-mesenchymal transition (EMT) in alveolar epithelial cells. It could coordinate with cigarette smoke extract (CSE) to promote proliferation of bronchial epithelial cells. In this study, we aim to explore the direct effect of IL-17A and CSE on EMT in bronchial epithelial cells.
methodsBronchial epithelial cells were isolated from C57BL/6 mice, and cocultured with CSE or/and IL-17A. E-cadherin and Vimentin expressions in cells were detected using immunofluorescence staining. IL-17R expression was detected using immunohistochemistry staining. NF-κB expression was assessed using western blotting. When NF-κB was inhibited by BAY 11-7821, expressions of NF-κB, E-cadherin and Vimentin were measured.
resultsThe protein expression of E-cadherin in bronchial epithelial cells was lowest in CSE + IL-17A group, followed by CSE group. In contrast, the protein expression of Vimentin was highest in CSE + IL-17A group, followed by CSE group. Similarly, IL-17R and NF-κB expressions were highest in CSE + IL-17A group, followed by CSE group and IL-17A group. NF-κB inhibitor could inhibit the expressions of E-cadherin and Vimentin.
conclusionsCigarette and IL-17A could synergistically induce EMT in bronchial epithelial cells through activating IL17R/NF-κB signaling. Our findings contribute to a better understanding in airway EMT and pathogenesis of respiratory diseases, which are involved IL-17A and cigarette smoking. Those will provide novel avenues in the immunotherapy of lung diseases.
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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.