ArticleMucosal immunology2012
Mucus clearance, MyD88-dependent and MyD88-independent immunity modulate lung susceptibility to spontaneous bacterial infection and inflammation.
Article in Mucosal immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
61 citing papers in PubMed, 85 citations in OpenAlex.
- SARS-CoV-2 infection produces an IL-33-dependent chronic eosinophilic pneumonia and muco-inflammatory airways disease in Scnn1b-Tg mice.JCI insight · 2026Article
- The MEK inhibitor trametinib incurs mitochondrial injury and induces innate immune responses in the mouse heart.Science advances · 2026Article
- Preventive intrapulmonary treatment withERJ open research · 2026Article
- Myeloid cell-specific HMGB1 deficiency exaggerates mucoinflammatory responses but promotes bacterial clearance in mucoinflammatory lung disease.Scientific reports · 2026Article
- The microbiome and gut-lung axis in nontuberculous mycobacterial pulmonary disease.PLoS pathogens · 2025Review
- The MEK inhibitor trametinib incurs mitochondrial injury and induces innate immune responses in the mouse heart.bioRxiv : the preprint server for biology · 2025Article
- Combustion products of burn pit constituents induce more changes in asthmatic than non-asthmatic murine lungs.Particle and fibre toxicology · 2025Article
- Interleukin-1 and Interleukin-8 are Prominent Inflammatory Markers in Patients with Cystic Fibrosis and Non-Cystic Fibrosis.Tanaffos · 2025Article
- Pulmonary-delivered Anticalin Jagged-1 antagonists reduce experimental airway mucus hyperproduction and obstruction.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Airway epithelial cell-specific deletion of EGFR modulates mucoinflammatory features of cystic fibrosis-like lung disease in mice.Frontiers in immunology · 2025Article
- Chronic hyperglycemia aggravates lung function in aAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
- Airway Inflammation in Children with Primary Ciliary Dyskinesia.Annals of the American Thoracic Society · 2023Observational
- The changing landscape of the cystic fibrosis lung environment: From the perspective of Pseudomonas aeruginosa.Current opinion in pharmacology · 2022Review
- Animal models of cystic fibrosis in the era of highly effective modulator therapies.Current opinion in pharmacology · 2022Review
- Chronic Allergen Challenge Induces Corticosteroid Insensitivity With Persistent Airway Remodeling and Type 2 Inflammation.Frontiers in pharmacology · 2022Article
- Airway epithelial cell-specific deletion of HMGB1 exaggerates inflammatory responses in mice with muco-obstructive airway disease.Frontiers in immunology · 2022Article
- Corticosteroid insensitivity persists in the absence of STAT1 signaling in severe allergic airway inflammation.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Epigenetic reprogramming of airway macrophages promotes polarization and inflammation in muco-obstructive lung disease.Nature communications · 2021Article
- Induction of IL-12p40 and type 1 immunity by Toxoplasma gondii in the absence of the TLR-MyD88 signaling cascade.PLoS pathogens · 2021Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
It has been postulated that mucus stasis is central to the pathogenesis of obstructive lung diseases. In Scnn1b-transgenic (Scnn1b-Tg⁺ mice, airway-targeted overexpression of the epithelial Na⁺ channel β subunit causes airway surface dehydration, which results in mucus stasis and inflammation. Bronchoalveolar lavage from neonatal Scnn1b-Tg⁺ mice, but not wild-type littermates, contained increased mucus, bacteria, and neutrophils, which declined with age. Scnn1b-Tg⁺ mice lung bacterial flora included environmental and oropharyngeal species, suggesting inhalation and/or aspiration as routes of entry. Genetic deletion of the Toll-interleukin-1 receptor adapter molecule MyD88 in Scnn1b-Tg⁺ mice did not modify airway mucus obstruction, but caused defective neutrophil recruitment and increased bacterial infection, which persisted into adulthood. Scnn1b-Tg⁺ mice derived into germ-free conditions exhibited mucus obstruction similar to conventional Scnn1b-Tg⁺ mice and sterile inflammation. Collectively, these data suggest that dehydration-induced mucus stasis promotes infection, compounds defects in other immune mechanisms, and alone is sufficient to trigger airway inflammation.
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Registered trials
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.