ArticleScientific reports2019
HDAC6 depletion improves cystic fibrosis mouse airway responses to bacterial challenge.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 30 citations in OpenAlex.
- HDAC6 inhibition reducesInfection and immunity · 2026Article
- A longitudinal evaluation of localised chronic Pseudomonas aeruginosa infection in cystic fibrosis rat models.BMC microbiology · 2026Article
- Extracellular Particles Derived From Mesenchymal Stromal Cells ReduceJournal of extracellular biology · 2026Article
- The role of HDAC6 in fibrosis: a novel and effective therapy strategy.European journal of medical research · 2025Review
- Comparison of artificial intelligence image processing with manual leucocyte differential to score immune cell infiltration in a mouse infection model of cystic fibrosis.Journal of pathology informatics · 2025Article
- Efficacy of melatonin treatment in a cystic fibrosis mouse model of airway infection.Scientific reports · 2025Article
- The role of HDAC6 in enhancing macrophage autophagy via the autophagolysosomal pathway to alleviate legionella pneumophila-induced pneumonia.Virulence · 2024Article
- A New Frontier in Cystic Fibrosis Pathophysiology: How and When Clock Genes Can Affect the Inflammatory/Immune Response in a Genetic Disease Model.Current issues in molecular biology · 2024Review
- Preclinical murine models for the testing of antimicrobials against Mycobacterium abscessus pulmonary infections: Current practices and recommendations.Tuberculosis (Edinburgh, Scotland) · 2024Review
- Extracellular vesicles secreted by primary human bronchial epithelial cells reduceAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Unveiling the modulation ofFrontiers in microbiology · 2024Article
- A minimally invasive bronchoscopic approach for direct delivery to murine airways and application to models of pulmonary infection.Laboratory animals · 2023Article
- Deacetylation of Histones and Non-histone Proteins in Inflammatory Diseases and Cancer Therapeutic Potential of Histone Deacetylase Inhibitors.Current genomics · 2023Review
- In vivo impact of tubulin polymerization promoting protein (Tppp) knockout to the airway inflammatory response.Scientific reports · 2023Article
- To bead or not to bead: A review ofFrontiers in physiology · 2023Review
- The circadian system in cystic fibrosis mice is regulated by histone deacetylase 6.American journal of physiology. Cell physiology · 2022Article
- Recruitment of monocytes primed to express heme oxygenase-1 ameliorates pathological lung inflammation in cystic fibrosis.Experimental & molecular medicine · 2022Article
- Carbonic anhydrase and soluble adenylate cyclase regulation of cystic fibrosis cellular phenotypes.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Chasing a Breath of Fresh Air in Cystic Fibrosis (CF): Therapeutic Potential of Selective HDAC6 Inhibitors to Tackle Multiple Pathways in CF Pathophysiology.Journal of medicinal chemistry · 2022Review
- Role of Histone Post-Translational Modifications in Inflammatory Diseases.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The hypothesis of this study was that Hdac6 depletion would restore cystic fibrosis (CF) responses to bacterial challenge to more wild type profiles using a CF mouse model. CF mice harboring the F508del Cftr mutation respond to bacterial challenge with 25,000 CFU Pseudomonas aeruginosa embedded into agarose beads to slow clearance. CF mice respond significantly more aggressively to this challenge compared to WT mice with respect to bacterial clearance, weight loss, neutrophil recruitment, and MIP-2 production. Depletion of Hdac6 expression in the CF mice (CF/Hdac6) significantly improves these responses to more WT levels. Weight loss in response to infection is most severe in CF mice and significantly attenuated in CF/Hdac6 mice. Bacterial levels are reduced at a faster rate in CF/Hdac6 mice compared to CF mice where infection persists. Percent neutrophils in lung lavage fluid post-infection are significantly higher in CF mice, but returned to WT levels with CF/Hdac6 mice. Similarly, CF Mip-2 levels are restored to WT levels in the absence of Hdac6 expression. These data demonstrate that Hdac6 depletion restores CF responses to bacterial challenge to WT-like profiles and offer a potential therapeutic avenue for addressing inflammation and infection in CF airways independently of Cftr correction.
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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.