ArticlePloS one2023
Nucleic acid sensor STING drives remodeling and its inhibition enhances steroid responsiveness in chronic obstructive pulmonary disease.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- STING pathway contributes to Steroid-Hyporesponsive Lung Inflammation in DSS-induced colitis mice model.PloS one · 2026Article
- The cGAS-STING Pathway in Pulmonary Diseases: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and adulthood.Biochemical and biophysical research communications · 2025Article
- Calprotectin inhibition attenuates silica-induced lung fibrosis.Inflammopharmacology · 2025Article
- cGAS-STING targeting offers therapy choice in lung diseases.Biology direct · 2025Review
- A combination of silica and cigarette smoke extract exacerbates lung fibrosis: Unveiling a harmful synergy.PloS one · 2025Article
- Calprotectin is regulated by IL-17A and induces steroid hyporesponsiveness in asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Emerging therapeutic targets in systemic sclerosis.Journal of molecular medicine (Berlin, Germany) · 2024Review
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic obstructive pulmonary disease (COPD) is progressive and irreversible chronic lung inflammatory disease. Cigarette smoke, the main cause of COPD, is often associated with double-stranded DNA release which potentially activates DNA-sensing pathways, such as STING. This study, therefore, analyzed the role of STING pathway in inducing pulmonary inflammation, steroid resistance, and remodeling in COPD.
methodsPrimary cultured lung fibroblasts were isolated from healthy non-smoker, healthy smoker, and smoker COPD individuals. The expression of STING pathway, remodeling, and steroid resistance signatures were investigated in these fibroblasts upon LPS stimulation and treatment with dexamethasone and/or STING inhibitor, at both mRNA and protein levels using qRT-PCR, western blot, and ELISA.
resultsAt baseline, STING was elevated in healthy smoker fibroblasts and to a higher extent in smoker COPD fibroblasts when compared to healthy non-smoker fibroblasts. Upon using dexamethasone as monotherapy, STING activity was significantly inhibited in healthy non-smoker fibroblasts but showed resistance in COPD fibroblasts. Treating both healthy and COPD fibroblasts with STING inhibitor in combination with dexamethasone additively inhibited STING pathway in both groups. Moreover, STING stimulation triggered a significant increase in remodeling markers and a reduction in HDAC2 expression. Interestingly, treating COPD fibroblasts with the combination of STING inhibitor and dexamethasone alleviated remodeling and reversed steroid hyporesponsiveness through an upregulation of HDAC2.
conclusionThese findings support that STING pathway plays an important role in COPD pathogenesis, via inducing pulmonary inflammation, steroid resistance, and remodeling. This raises the possibility of using STING inhibitor as a potential therapeutic adjuvant in combination with common steroid treatment.
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