ArticleBMC pulmonary medicine2008
Effect of roflumilast on inflammatory cells in the lungs of cigarette smoke-exposed mice.
Article in BMC pulmonary medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 46 citations in OpenAlex.
- Roflumilast prevented tissue damage caused by lipopolysaccharide-induced sepsis via anti-inflammatory action.PloS one · 2026Article
- Clinical Implication of Phosphodiesterase-4-Inhibition.International journal of molecular sciences · 2022Review
- Scope of adjuvant therapy using roflumilast, a PDE-4 inhibitor against COVID-19.Pulmonary pharmacology & therapeutics · 2021Review
- Bacterial-derived Neutrophilic Inflammation Drives Lung Remodeling in a Mouse Model of Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2018Article
- The Phosphodiesterase 4 Inhibitor Roflumilast Protects against Cigarette Smoke Extract-Induced Mitophagy-Dependent Cell Death in Epithelial Cells.Tuberculosis and respiratory diseases · 2018Article
- Lung Macrophage Phenotypes and Functional Responses: Role in the Pathogenesis of COPD.International journal of molecular sciences · 2018Review
- Airway bacteria drive a progressive COPD-like phenotype in mice with polymeric immunoglobulin receptor deficiency.Nature communications · 2016Article
- Roflumilast partially reverses smoke-induced mucociliary dysfunction.Respiratory research · 2015Article
- Roflumilast inhibits lipopolysaccharide-induced tumor necrosis factor-α and chemokine production by human lung parenchyma.PloS one · 2013Article
- Roflumilast inhibits the release of chemokines and TNF-α from human lung macrophages stimulated with lipopolysaccharide.British journal of pharmacology · 2012Article
- Impact of smoking on inflammation: overview of molecular mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Review
- Update on roflumilast, a phosphodiesterase 4 inhibitor for the treatment of chronic obstructive pulmonary disease.British journal of pharmacology · 2011Review
- Roflumilast, a Novel Phosphodiesterase 4 Inhibitor, for COPD Patients with a History of Exacerbations.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2011Article
- New therapeutic options in the management of COPD - focus on roflumilast.International journal of chronic obstructive pulmonary disease · 2011Review
- Roflumilast: first phosphodiesterase 4 inhibitor approved for treatment of COPD.Drug design, development and therapy · 2010Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe reported that roflumilast, a phosphodiesterase 4 inhibitor, given orally at 5 mg/kg to mice prevented the development of emphysema in a chronic model of cigarette smoke exposure, while at 1 mg/kg was ineffective. Here we investigated the effects of roflumilast on the volume density (VV) of the inflammatory cells present in the lungs after chronic cigarette smoke exposure.
methodsSlides were obtained from blocks of the previous study and VV was assessed immunohistochemically and by point counting using a grid with 48 points, a 20x objective and a computer screen for a final magnification of 580x. Neutrophils were marked with myeloperoxidase antibody, macrophages with Mac-3, dendritic cells with fascin, B-lymphocytes with B220, CD4+ T-cells with CD4+ antibody, and CD8+T-cells with CD8-alpha. The significance of the differences was calculated using one-way analysis of variance.
resultsChronic smoke exposure increased neutrophil VV by 97%, macrophage by 107%, dendritic cell by 217%, B-lymphocyte by 436%, CD4+ by 524%, and CD8+ by 417%. The higher dose of roflumilast prevented the increase in neutrophil VV by 78%, macrophage by 82%, dendritic cell by 48%, B-lymphocyte by 100%, CD4+ by 98% and CD8+ VV by 88%. The lower dose of roflumilast did not prevent the increase in neutrophil, macrophage and B-cell VV but prevented dendritic cells by 42%, CD4+ by 55%, and CD8+ by 91%.
conclusionThese results indicate (i) chronic exposure to cigarette smoke in mice results in a significant recruitment into the lung of inflammatory cells of both the innate and adaptive immune system; (ii) roflumilast at the higher dose exerts a protective effect against the recruitment of all these cells and at the lower dose against the recruitment of dendritic cells and T-lymphocytes; (iii) these findings underline the role of innate immunity in the development of pulmonary emphysema and (iiii) support previous results indicating that the inflammatory cells of the adaptive immune system do not play a central role in the development of cigarette smoke induced emphysema in mice.
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