ArticleRespiratory research2014
Combined exposure to cigarette smoke and nontypeable Haemophilus influenzae drives development of a COPD phenotype in mice.
Article in Respiratory research, 2014. 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- The Human Respiratory Microbiome: Current Understandings and Future Directions.American journal of respiratory cell and molecular biology · 2023Pooled it
- Muc16 contributes to protection against invasive pneumococcal infection originating from nasal colonization.Microbiology spectrum · 2026Article
- Quercetin in COPD: A Multi-Target Approach to Modulate Inflammation, Oxidative Stress, and Epithelial Dysfunction.International journal of molecular sciences · 2026Review
- Muscle-lung crosstalk in COPD: how exercise training modulates protein metabolism and inflammation in experimental COPD models.Frontiers in immunology · 2026Review
- Short-term cigarette smoke exposure aggravates oxidative stress and airway inflammation induced by lipopolysaccharides.Frontiers in physiology · 2026Article
- An update in club cell biology and its potential relevance to chronic obstructive pulmonary disease.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- Closing the Loop on the Vicious Circle in Chronic Obstructive Pulmonary Disease.Annals of the American Thoracic Society · 2022Article
- Effects of repeated infections with non-typeable Haemophilus influenzae on lung in vitamin D deficient and smoking mice.Respiratory research · 2022Article
- Article
- Neutrophil Elastase and Chronic Lung Disease.Biomolecules · 2021Review
- FOXO3a regulates rhinovirus-induced innate immune responses in airway epithelial cells.Scientific reports · 2019Article
- Repeated Exposure to Streptococcus pneumoniae Exacerbates Chronic Obstructive Pulmonary Disease.The American journal of pathology · 2019Article
- Rhinovirus-induces progression of lung disease in a mouse model of COPD via IL-33/ST2 signaling axis.Clinical science (London, England : 1979) · 2019Article
- The pathology of small airways disease in COPD: historical aspects and future directions.Respiratory research · 2019Review
- The Interplay Between Immune Response and Bacterial Infection in COPD: Focus Upon Non-typeableFrontiers in immunology · 2018Review
- Quercetin prevents rhinovirus-induced progression of lung disease in mice with COPD phenotype.PloS one · 2018Article
- The Role of Regulatory T Cell in NontypeableMediators of inflammation · 2018Article
- Rhinovirus and COPD airway epithelium.Pulmonary and critical care medicine · 2017Article
- Immune-mediated inflammation in the pathogenesis of emphysema: insights from mouse models.Cell and tissue research · 2017Review
- Interleukin-22 protects against non-typeable Haemophilus influenzae infection: alteration during chronic obstructive pulmonary disease.Mucosal immunology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCigarette smoke (CS) is the major etiologic factor of chronic obstructive pulmonary disease (COPD). CS-exposed mice develop emphysema and mild pulmonary inflammation but no airway obstruction, which is also a prominent feature of COPD. Therefore, CS may interact with other factors, particularly respiratory infections, in the pathogenesis of airway remodeling in COPD.
methodsC57BL/6 mice were exposed to CS for 2 h a day, 5 days a week for 8 weeks. Mice were also exposed to heat-killed non-typeable H. influenzae (HK-NTHi) on days 7 and 21. One day after the last exposure to CS, mice were sacrificed and lung inflammation and mechanics, emphysematous changes, and goblet cell metaplasia were assessed. Mice exposed to CS or HK-NTHi alone or room air served as controls. To determine the susceptibility to viral infections, we also challenged these mice with rhinovirus (RV).
resultsUnlike mice exposed to CS or HK-NTHi alone, animals exposed to CS/HK-NTHi developed emphysema, lung inflammation and goblet cell metaplasia in both large and small airways. CS/HK-NTHi-exposed mice also expressed increased levels of mucin genes and cytokines compared to mice in other groups. CS/HK-NTHi-exposed mice infected with RV demonstrated increased viral persistence, sustained neutrophilia, and further increments in mucin gene and chemokine expression compared to other groups.
conclusionsThese findings indicate that in addition to CS, bacteria may also contribute to development of COPD, particularly changes in airways. Mice exposed to CS/HK-NTHi are also more susceptible to subsequent viral infection than mice exposed to either CS or HK-NTHi alone.
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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.