ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Compromised respiratory function in lethal influenza infection is characterized by the depletion of type I alveolar epithelial cells beyond threshold levels.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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53 citing papers in PubMed, 70 citations in OpenAlex.
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- TLR7 deficiency enhances inflammation in the URT but reduces LRT immunity following influenza A infection.Scientific reports · 2025Article
- ZBP1-driven cell death in severe influenza.Trends in microbiology · 2025Review
- Perinatal Nicotine Exposure Disrupts Hematopoietic Stem Cell Development and Elevates Influenza Susceptibility in Adulthood.bioRxiv : the preprint server for biology · 2025Article
- Evaluation of intranasal TLR2/6 agonist INNA-051: safety, tolerability and proof of pharmacology.ERJ open research · 2024Article
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- Immune response in influenza virus infection and modulation of immune injury by viral neuraminidase.Virology journal · 2023Review
- Transcriptome-wide 5-methylcytosine modification profiling of long non-coding RNAs in A549 cells infected with H1N1 influenza A virus.BMC genomics · 2023Article
- ZBP1/DAI-Dependent Cell Death Pathways in Influenza A Virus Immunity and Pathogenesis.Current topics in microbiology and immunology · 2023Article
- Capillary Blood Gas in Children Hospitalized Due to Influenza Predicts the Risk of Lower Respiratory Tract Infection.Diagnostics (Basel, Switzerland) · 2022Article
- Review
- Surfactant protein D is a biomarker of influenza-related pediatric lung injury.Pediatric pulmonology · 2022Article
- Innate immune sensing of influenza A viral RNA through IFI16 promotes pyroptotic cell death.iScience · 2022Article
- The Mechanism behind Influenza Virus Cytokine Storm.Viruses · 2021Review
- Influenza virus and SARS-CoV-2: pathogenesis and host responses in the respiratory tract.Nature reviews. Microbiology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
During influenza virus infection, it is unclear how much alveolar cell loss can be tolerated before the host succumbs to the disease. We sought to define relevant correlates of disease severity in the mouse influenza model, hypothesizing that a susceptibility threshold exists for alveolar epithelial cell loss. We compared lung pathology, virus spread, alveolar epithelial cell depletion, arterial blood oxygenation, physiological responses measured by unrestrained plethysmography, and oxygen consumption and carbon dioxide production by gas analysis in mice at intervals after infection with virus strains and doses that cause mild (x31) or severe (PR/8) influenza. Both mild and severe infections showed similar degrees of lung damage and virus dissemination until day 6 after inoculation but diverged in survival outcomes from day 9. Day 6 PR/8-infected mice had normal respiratory and gas exchange functions with 10% type I cell loss. However, day 10 PR/8-infected mice had 40% type I cell loss with a concomitant drastic decreases in tidal and minute volumes, Vo(2), Vco(2), and arterial blood oxygenation, compared with a maximum 3% type I cell loss for x31 on day 10 when they recovered body weight and respiratory functions. Alterations in breaths per minute, expiratory time, and metabolic rate were observed in both infections. A threshold for maintenance of proper respiratory function appears to be crossed once 10% of alveolar type I cells are lost. These data indicate that lethality in influenza virus infection is a matter of degree rather than quality.
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