ArticleFrontiers in immunology2017
Stimulator of Interferon Genes Deficiency in Acute Exacerbation of Idiopathic Pulmonary Fibrosis.
Article in Frontiers in immunology, 2017. 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, 27 citations in OpenAlex.
- Murine models of pulmonary fibrosis: mechanisms, limitations and translational insights.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Immunosenescence in Idiopathic Pulmonary Fibrosis.Journal of inflammation research · 2026Review
- Variable steady inflammation and inflammatory responses in precision-cut lung slices from various IPF lung Regions.Respiratory research · 2025Article
- The cGAS-STING Pathway in Pulmonary Diseases: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.Frontiers in pharmacology · 2025Review
- Review
- Article
- The immune mechanisms of acute exacerbations of idiopathic pulmonary fibrosis.Frontiers in immunology · 2024Review
- Non-Interferon-Dependent Role of STING Signaling in Pulmonary Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Animal models of acute exacerbation of pulmonary fibrosis.Respiratory research · 2023Review
- STING Targeting in Lung Diseases.Cells · 2022Review
- Essential role of IL-17 in acute exacerbation of pulmonary fibrosis induced by non-typeableTheranostics · 2022Article
- The cGAS-STING pathway: more than fighting against viruses and cancer.Cell & bioscience · 2021Review
- Selenium Supplementation Protects Against Lipopolysaccharide-Induced Heart Injury via Sting Pathway in Mice.Biological trace element research · 2021Article
- Article
- STING Signaling and Sterile Inflammation.Frontiers in immunology · 2021Review
- Serum mitochondrial DNA predicts the risk of acute exacerbation and progression of idiopathic pulmonary fibrosis.The European respiratory journal · 2021Article
- ILDGDB: a manually curated database of genomics, transcriptomics, proteomics and drug information for interstitial lung diseases.BMC pulmonary medicine · 2020Article
- Protective Role of the Nucleic Acid Sensor STING in Pulmonary Fibrosis.Frontiers in immunology · 2020Article
- IL-17A contributes to HSV1 infection-induced acute lung injury in a mouse model of pulmonary fibrosis.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The stimulator of interferon genes (STING) is a key adaptor protein mediating innate immune defense against DNA viruses. To investigate the role of STING in acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF), we isolated primary peripheral blood mononuclear cells (PBMCs) from patients and healthy controls (HCs). Raw264.7 and A549 cells were infected with herpes simplex virus type 1 (HSV-1). Mice with bleomycin-induced lung fibrosis were infected with HSV-1 to stimulate acute exacerbation of the lung fibrosis. Global gene expression profiling revealed a substantial downregulation of interferon-regulated genes (downstream of STING) in the AE-IPF group compared with the HC and stable IPF groups. The PBMCs of the AE-IPF group showed significantly reduced STING protein levels, increased levels of endoplasmic reticulum (ER) stress markers, and elevated apoptosis. HSV-1 infection decreased STING expression and stimulated the ER stress pathways in Raw264.7 and A549 cells in a time- and dose-dependent manner. HSV-1 infection exacerbated the bleomycin-induced lung injury in mice. In the primary bone marrow-derived macrophages of mice treated with bleomycin and HSV-1, STING protein expression was substantially reduced; ER stress was stimulated. Tauroursodeoxycholic acid, a known inhibitor of ER stress, partially reversed those HSV-1-mediated adverse effects in mice with bleomycin-induced lung injury. STING levels in PBMCs increased after treatment in patients showing improvement but remained at low levels in patients with deterioration. Viral infection may trigger ER stress, resulting in STING deficiency and AE-IPF onset.
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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.