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Research Article Free access | 10.1172/JCI107484
1Pulmonary Unit, Department of Medicine, and the Specialized Center of Research in Pulmonary Diseases (SCOR), University of Vermont College of Medicine, Burlington, Vermont 05401
Find articles by Jakab, G. in: JCI | PubMed | Google Scholar
1Pulmonary Unit, Department of Medicine, and the Specialized Center of Research in Pulmonary Diseases (SCOR), University of Vermont College of Medicine, Burlington, Vermont 05401
Find articles by Green, G. in: JCI | PubMed | Google Scholar
Published November 1, 1973 - More info
Bacterial multiplication in the lung associated with murine Sendai virus pneumonia is caused by virus-induced defects in pulmonary bactericidal mechanisms. The nature of this effect has been studied in animals immunized against the challenge bacteria. Mice were immunized against Proteus mirabilis by intraperitoneal inoculation and by aerosol inhalation. After the development of immunity, mice were infected aerogenically with 104 TCID50 of Sendai virus. 7 days later, during the height of the bronchial inflammation and pulmonary consolidation, the mice were challenged with an aerosol of viable 35S-labeled Proteus mirabilis or 32P-labeled Staphylococcus aureus.
Nonimmunized virus-infected animals showed marked impairment of pulmonary bactericidal activity with subsequent multiplication of the bacterial strain in the case of Proteus mirabilis. Immunized nonvirus-infected animals showed enhancement of pulmonary bactericidal activity for the homologous and heterologous strains in comparison with nonimmunized animals. Virus-infected animals immunized by aerosol showed enhanced bactericidal activity against the homologous but not the heterologous bacterial strain. Neither virus infection nor immunization had a significant effect on the transport of particles in the lung. The data demonstrated that the bacterial multiplication associated with the virus pneumonia was prevented by preceding immunization against the homologous challenge organism. The data suggest a mechanism for controlling bacterial multiplication associated with virus pneumonias.