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Chronic ethanol ingestion in mice enhances influenza A H1N1 pulmonary lesions
Author(s) -
Meyerholz David K.,
Edsen Michelle,
Coleman Ruth A.,
Cook Robert T.,
Legge Kevin L.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a9-a
Subject(s) - medicine , lung , atelectasis , pathology , bronchiolitis , pneumonia , pulmonary edema , immune system , diffuse alveolar damage , respiratory disease , viral pneumonia , immunology , virus , covid-19 , acute respiratory distress , disease , infectious disease (medical specialty)
Chronic ethanol ingestion leads to immunological alterations of both the innate and adaptive immune systems and is suggested to contribute, in part, toward the increased susceptibility to and severity of community acquired pneumonia. In this pilot study, C57Bl/6 mice treated for 4 weeks with 20% ethanol‐in‐water (w/v) as the only source water, and matched controls were infected with a lethal dose of influenza A/PR/8/34 H1N1 (200 EIU/mouse). At days four and five post‐inoculation (PI), the mice were euthanized, lung tissue formalin‐fixed and processed for histopathological examination. There was no significant difference at day four, and pulmonary lesions consisted of necrotizing bronchiolitis with perivascular edema and cellular infiltrate that extended into the alveolar septa. By day five PI, lesions in the chronic ethanol treated mice were more widespread and severe. Necrotizing bronchiolitis was present in a larger fraction of the lung lobes and severe neutrophilic infiltrates effaced many airways structures. Lobar consolidation was accentuated by severe alveolar flooding of seroproteinaceous fluid, cellular infiltrate and atelectasis. Two mechanisms of increased pulmonary lesions are suggested by this study, chronic ethanol exposure may increase viral titers, or alter the immune system predisposing the lung to increased damage. Supported by NIH AA‐014405 and the UI Department of Pathology.