Influenza virus infection, ozone exposure, and fibrogenesis

Journal Article · Tue May 01 00:00:00 EDT 1990 · American Review of Respiratory Disease (New York); (USA)

DOI:https://doi.org/10.1164/ajrccm/141.5_Pt_1.1307· OSTI ID:6742584

Jakab, G J; Bassett, D J ^[1]

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1. Johns Hopkins School of Hygiene and Public Health, Baltimore, MD (USA)

Oxidant exposure following chemically induced lung injury exacerbates the tendency to develop pulmonary fibrosis. Influenza virus pneumonitis causes severe acute lung damage that, upon resolution, is followed by a persistent alveolitis and parenchymal changes characterized by patchy interstitial pneumonia and collagen deposition in the affected areas. To determine whether oxidant exposure exacerbates the virus-induced alveolitis and residual lung damage, mice were infected by aerosol inhalation with influenza A virus and continuously exposed to 0.5 ppm ozone or ambient air. Noninfected control mice were exposed to either ambient air or ozone. On various days during the first month after infection, groups of mice were sacrificed and their lungs assessed for acute injury (lung lavage albumin, total and differential cell counts, wet/dry ratios, and morphometry). At 30, 60, 90, and 120 days after infection, groups of mice were sacrificed for total and differential lavage cell counts, lung hydroxyproline content, and morphometric analysis. Ozone exposure did not alter the proliferation of virus in the lungs as quantitated by infectious virus titers of lung homogenates at 1, 4, 7, 10, and 15 days after virus infection but mitigated the virus-induced acute lung injury by approximately 50%. After Day 30 a shift in the character of the pulmonary lesions was observed in that continuous exposure to ozone potentiated the postinfluenzal alveolitis and structural changes in the lung parenchyma. Additional studies suggest that the mechanism for the enhanced postinfluenzal lung damage may be related to the oxidant impairing the repair process of the acute influenzal lung damage. These data demonstrate that ozone exposure mitigates acute virus-induced lung injury and potentiates residual lung damage.

• OSTI ID: 6742584
• Journal Information: American Review of Respiratory Disease (New York); (USA), Journal Name: American Review of Respiratory Disease (New York); (USA) Vol. 141; ISSN ARDSB; ISSN 0003-0805
• Country of Publication: United States
• Language: English

Related Subjects

560300* -- Chemicals Metabolism & Toxicology
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
AIR POLLUTION
ALBUMINS
AMINES
AMINO ACIDS
ANIMALS
AZOLES
BODY
CARBOXYLIC ACIDS
CELL PROLIFERATION
DISEASES
FIBROSIS
HETEROCYCLIC ACIDS
HETEROCYCLIC COMPOUNDS
HYDROXY ACIDS
HYDROXYPROLINE
INFECTIOUS DISEASES
INFLUENZA
INFLUENZA VIRUSES
INHALATION
INHIBITION
INTAKE
LAVAGE
LUNGS
MAMMALS
MICE
MICROORGANISMS
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANIC NITROGEN COMPOUNDS
ORGANS
OZONE
PARASITES
PATHOLOGICAL CHANGES
POLLUTION
PROTEINS
PYRROLES
PYRROLIDINES
RESPIRATORY SYSTEM
RODENTS
TOXICITY
VERTEBRATES
VIRAL DISEASES
VIRUSES