ArticleRespiratory research2011
Acute intratracheal Pseudomonas aeruginosa infection in cystic fibrosis mice is age-independent.
Article in Respiratory research, 2011. 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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15 citing papers in PubMed, 35 citations in OpenAlex.
- Increased NFAT and NFκB signalling contribute to the hyperinflammatory phenotype in response to Aspergillus fumigatus in a mouse model of cystic fibrosis.PLoS pathogens · 2025Article
- Cystic Fibrosis Mice Are Highly Susceptible to Repeated AcuteBioMed research international · 2024Article
- Acute polymicrobial airway infections: analysis in cystic fibrosis mice.Microbiology (Reading, England) · 2023Article
- To bead or not to bead: A review ofFrontiers in physiology · 2023Review
- Proteobacteria and Firmicutes Secreted Factors Exert Distinct Effects onMetabolites · 2022Article
- AnF1000Research · 2021Article
- Article
- Lung infection caused by Pseudomonas aeruginosa in a CD26/DPP4 deficient F344 rat model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- Pathogenesis of Respiratory Syncytial Virus Infection in BALB/c Mice Differs Between Intratracheal and Intranasal Inoculation.Viruses · 2019Article
- Anti-inflammatory effect of Yu-Ping-Feng-SanIranian journal of basic medical sciences · 2016Article
- Pseudomonas toxin pyocyanin triggers autophagy: Implications for pathoadaptive mutations.Autophagy · 2016Article
- Elastin degradation product isodesmosine is a chemoattractant for Pseudomonas aeruginosa.Microbiology (Reading, England) · 2015Article
- Article
- Ventilatory pattern and energy expenditure are altered in cystic fibrosis mice.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2013Article
- Efficacy and safety of liposomal clarithromycin and its effect on Pseudomonas aeruginosa virulence factors.Antimicrobial agents and chemotherapy · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSince the discovery of the human CFTR gene in 1989 various mouse models for cystic fibrosis (CF) have been generated and used as a very suitable and popular tool to approach research on this life-threatening disease. Age related changes regarding the course of disease and susceptibility towards pulmonary infections have been discussed in numerous studies.
methodsHere, we investigated CftrTgH(neoim)Hgu and Cftrtm1Unc-Tg(FABPCFTR)1Jaw/J CF mice and their non-CF littermates during an acute lung infection with Pseudomonas aeruginosa for age dependent effects of their lung function and immune response.Mice younger than three or older than six months were intratracheally infected with P. aeruginosa TBCF10839. The infection was monitored by lung function of the animals using non-invasive head-out spirometry and the time course of physiological parameters over 192 hours. Quantitative bacteriology and lung histopathology of a subgroup of animals were used as endpoint parameters.
resultsAge-dependent changes in lung function and characteristic features for CF like a shallower, faster breathing pattern were observed in both CF mouse models in uninfected state. In contrast infected CF mice did not significantly differ from their non-CF littermates in susceptibility and severity of lung infection in both mouse models and age groups. The transgenic Cftrtm1Unc-Tg(FABPCFTR)1Jaw/J and their non-CF littermates showed a milder course of infection than the CftrTgH(neoim)Hgu CF and their congenic C57Bl/6J non-CF mice suggesting that the genetic background was more important for outcome than Cftr dysfunction.
conclusionsPrevious investigations of the same mouse lines have shown a higher airway susceptibility of older CF mice to intranasally applied P. aeruginosa. The different outcome of intranasal and intratracheal instillation of bacteria implies that infected CF epithelium is impaired during the initial colonization of upper airways, but not in the subsequent response of host defense.
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