ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Infection of mice with influenza A/WSN/33 (H1N1) virus alters alveolar type II cell phenotype.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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, 28 citations in OpenAlex.
- Differences in glycolytic metabolism between tissue-resident alveolar macrophages and recruited lung macrophages.Frontiers in immunology · 2025Review
- Article
- Article
- Cytidine 5'-Diphosphocholine Corrects Alveolar Type II Cell Mitochondrial Dysfunction in Influenza-infected Mice.American journal of respiratory cell and molecular biology · 2022Article
- Impact of cytidine diphosphocholine on oxygenation in client-owned dogs with aspiration pneumonia.Journal of veterinary internal medicine · 2022Article
- Postexposure Liponucleotide Prophylaxis and Treatment Attenuates Acute Respiratory Distress Syndrome in Influenza-infected Mice.American journal of respiratory cell and molecular biology · 2021Article
- Lung Epithelial Cell Transcriptional Regulation as a Factor in COVID-19-associated Coagulopathies.American journal of respiratory cell and molecular biology · 2021Article
- Liponucleotides: Promises and Unknowns as Novel Therapeutics for Acute Respiratory Distress Syndrome.American journal of respiratory cell and molecular biology · 2021Article
- Pulmonary Edema in COVID-19 Patients: Mechanisms and Treatment Potential.Frontiers in pharmacology · 2021Review
- Antiviral immune mechanism of Toll-like receptor 4-mediated human alveolar epithelial cells type Ⅱ.Experimental and therapeutic medicine · 2020Article
- Article
- The inducible amphisome isolates viral hemagglutinin and defends against influenza A virus infection.Nature communications · 2020Article
- Pulmonary function analysis in cotton rats after respiratory syncytial virus infection.PloS one · 2020Article
- A Three-Dimensional Human Tissue-Engineered Lung Model to Study Influenza A Infection.Tissue engineering. Part A · 2018Article
- Prion protein protects mice from lethal infection with influenza A viruses.PLoS pathogens · 2018Article
- ATP catabolism by tissue nonspecific alkaline phosphatase contributes to development of ARDS in influenza-infected mice.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Ion channels of the lung and their role in disease pathogenesis.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Influenza virus infection alters ion channel function of airway and alveolar cells: mechanisms and physiological sequelae.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Alternative Progenitor Lineages Regenerate the Adult Lung Depleted of Alveolar Epithelial Type 2 Cells.American journal of respiratory cell and molecular biology · 2017Article
- Lethal H1N1 influenza A virus infection alters the murine alveolar type II cell surfactant lipidome.American journal of physiology. Lung cellular and molecular physiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Influenza viruses cause acute respiratory disease of great importance to public health. Alveolar type II (ATII) respiratory epithelial cells are central to normal lung function and are a site of influenza A virus replication in the distal lung. However, the consequences of infection for ATII cell function are poorly understood. To determine the impact of influenza infection on ATII cells we used C57BL/6-congenic SP-C(GFP) mice that express green fluorescent protein (GFP) under the control of the surfactant protein-C (SP-C) promoter, which is only active in ATII cells. Most cells isolated from the lungs of uninfected SP-C(GFP) mice were GFP(+) but did not express the alveolar type I (ATI) antigen podoplanin (PODO). ATII cells were also EpCAM(+) and α2,3-linked sialosaccharide(+). Infection with influenza A/WSN/33 virus caused severe hypoxemia and pulmonary edema. This was accompanied by loss of whole lung GFP fluorescence, reduced ATII cell yields, increased ATII cell apoptosis, reduced SP-C gene and protein expression in ATII cell lysates, and increased PODO gene and protein levels. Flow cytometry indicated that infection decreased GFP(+)/PODO(-) cells and increased GFP(-)/PODO(+) and GFP(-)/PODO(-) cells. Very few GFP(+)/PODO(+) cells were detectable. Finally, infection resulted in a significant decline in EpCAM expression by PODO(+) cells, but had limited effects on α2,3-linked sialosaccharides. Our findings indicate that influenza infection results in a progressive differentiation of ATII cells into ATI-like cells, possibly via an SP-C(-)/PODO(-) intermediate, to replace dying or dead ATI cells. However, impaired SP-C synthesis is likely to contribute significantly to reduced lung compliance in infected mice.
Indexed as
Identifiers
What OpenQuestion holds
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.