ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
TLR9 expression is required for the development of cigarette smoke-induced emphysema in mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 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 elevated CXCL5 levels in circulation are associated with lung function decline in COPD patients and cigarette smoking-induced mouse model of COPD.Annals of medicineTrial
- Altered lung function in mice is a sensitive indicator of lung damage following 6 months of electronic nicotine delivery system aerosol exposure.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Proinflammatory monocyte-derived granulocyte-macrophage colony-stimulating factor fuels airway inflammation in bronchopulmonary dysplasia.Pediatric research · 2026Article
- Impact of Particulate Matter on the Exacerbation of Immunoglobulin A Nephropathy: An Animal Experimental Study.International journal of molecular sciences · 2025Article
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Article
- DNA of neutrophil extracellular traps promote NF-κB-dependent autoimmunity via cGAS/TLR9 in chronic obstructive pulmonary disease.Signal transduction and targeted therapy · 2024Article
- Identification of related-genes of T cells in lung tissue of chronic obstructive pulmonary disease based on bioinformatics and experimental validation.Scientific reports · 2024Article
- Mitochondrial damage-associated molecular patterns in chronic obstructive pulmonary disease: Pathogenetic mechanism and therapeutic target.Journal of translational internal medicine · 2023Article
- Protein Phosphatase 2A as a Therapeutic Target in Pulmonary Diseases.Medicina (Kaunas, Lithuania) · 2023Review
- An In Vitro Alveolar Model Allows for the Rapid Assessment of Particles for Respiratory Sensitization Potential.International journal of molecular sciences · 2023Article
- Identification of Genes Related to Endoplasmic Reticulum Stress (ERS) in Chronic Obstructive Pulmonary Disease (COPD) and Clinical Validation.International journal of chronic obstructive pulmonary disease · 2023Article
- Expanding role of deoxyribonucleic acid-sensing mechanism in the development of lifestyle-related diseases.Frontiers in cardiovascular medicine · 2022Review
- Oxidative Stress and Mitochondrial Damage in Dry Age-Related Macular Degeneration LikeBiology · 2021Article
- Phosphatases in toll-like receptors signaling: the unfairly-forgotten.Cell communication and signaling : CCS · 2021Review
- Article
- Self-DNA release and STING-dependent sensing drives inflammation to cigarette smoke in mice.Scientific reports · 2019Article
- Role of fibroblast growth factor 23 and klotho cross talk in idiopathic pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Fibroblast growth factor 23 and Klotho contribute to airway inflammation.The European respiratory journal · 2018Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The expression of Toll-like receptor (TLR)-9, a pathogen recognition receptor that recognizes unmethylated CpG sequences in microbial DNA molecules, is linked to the pathogenesis of several lung diseases. TLR9 expression and signaling was investigated in animal and cell models of chronic obstructive pulmonary disease (COPD). We observed enhanced TLR9 expression in mouse lungs following exposure to cigarette smoke. Tlr9(-/-) mice were resistant to cigarette smoke-induced loss of lung function as determined by mean linear intercept, total lung capacity, lung compliance, and tissue elastance analysis. Tlr9 expression also regulated smoke-mediated immune cell recruitment to the lung; apoptosis; expression of granulocyte-colony stimulating factor (G-CSF), the CXCL5 protein, and matrix metalloproteinase-2 (MMP-2); and protein tyrosine phosphatase 1B (PTP1B) activity in the lung. PTP1B, a phosphatase with anti-inflammatory abilities, was identified as binding to TLR9. In vivo delivery of a TLR9 agonist enhanced TLR9 binding to PTP1B, which inactivated PTP1B. Ptp1b(-/-) mice had elevated lung concentrations of G-CSF, CXCL5, and MMP-2, and tissue expression of type-1 interferon following TLR9 agonist administration, compared with wild-type mice. TLR9 responses were further determined in fully differentiated normal human bronchial epithelial (NHBE) cells isolated from nonsmoker, smoker, and COPD donors, and then cultured at air liquid interface. NHBE cells from smokers and patients with COPD expressed more TLR9 and secreted greater levels of G-CSF, IL-6, CXCL5, IL-1β, and MMP-2 upon TLR9 ligand stimulation compared with cells from nonsmoker donors. Although TLR9 combats infection, our results indicate that TLR9 induction can affect lung function by inactivating PTP1B and upregulating expression of proinflammatory cytokines.
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Registered trials
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