ArticleBioengineered2022
IL-35 inhibits cell pyroptosis and attenuates cell injury in TNF-α-induced bronchial epithelial cells via p38 MAPK signaling pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Impaired IL-35/Treg Axis Facilitates Neuropathic Pain Via TNF-α, TLR4, and HMGB1 Activation.Immunity, inflammation and disease · 2026Article
- Interleukin-35 as a key immunoregulatory mediator in steroid-hyporesponsive severe asthma.Frontiers in immunology · 2026Review
- IL-35 promotes IL-35Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Knockdown of KIF23 alleviates the progression of asthma by inhibiting pyroptosis.BMJ open respiratory research · 2024Article
- NJK14047 Suppression of the p38 MAPK Ameliorates OVA-Induced Allergic Asthma during Sensitization and Challenge Periods.Biomolecules & therapeutics · 2023Article
- Tanshinone IIA down-regulates -transforming growth factor beta 1 to relieve renal tubular epithelial cell inflammation and pyroptosis caused by high glucose.Bioengineered · 2022Article
- Inhibition of KIF23 Alleviates IPAH by Targeting Pyroptosis and Proliferation of PASMCs.International journal of molecular sciences · 2022Article
- Diosmetin attenuates oxidative stress-induced damage to lens epithelial cells via the mitogen-activated protein kinase (MAPK) pathway.Bioengineered · 2022Article
- The Molecular Role of IL-35 in Non-Small Cell Lung Cancer.Frontiers in oncology · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Asthma is a chronic inflammatory disease of the airways, and IL-35 has been found to be involved in the pathogenesis of inflammatory diseases by mediating the inhibition of effector T cells. But the role of IL-35 on cell pyroptosis, which frequently occurs in inflammatory diseases, has not been elucidated. Therefore, the present study used a TNF-α-induced bronchial epithelial cell injury model to investigate the mechanism of IL-35 action on cell pyroptosis and asthma injury. The effects of IL-35 on cell activity, inflammatory factor levels, cell barrier damage and cell pyroptosis-related proteins were examined by CCK-8, ELISA, lucifer yellow permeability and Western blotting assay, respectively. Subsequently, following the activation of p38 MAPK signaling pathway by adding p38 agonist, the effect of IL-35 on TNF-α-induced bronchial epithelial cell injury was investigated. The results showed that IL-35 reduced TNF-α-induced cell injury, decreased inflammatory factors, improved cell permeability, and inhibited cell pyroptosis. More importantly, the effect of IL-35 on injured cells was reversed after p38 MAPK pathway was activated. In summary, IL-35 inhibited p38 MAPK pathway to suppress cell pyroptosis and thereby reduce asthma injury.
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