Intrapulmonary antibacterial activity in normal mice and mice with viral pneumonia was determined after continuous exposure to the pure tobacco smoke component, acrolein. After inhalation challenge with Staphylococcus aureus and Proteus mirabilis, exposure to 1 to 2 ppm of acrolein significantly suppressed the intrapulmonary killing of the organisms in normal mice compared to control mice not exposed to acrolein. Sendai virus pneumonia depressed pulmonary antibacterial defenses in a virus dose related fashion. Exposure of the mice infected with virus to acrolein resulted in a further suppression of intrapulmonary bacterial killing to the extent that, in most instances, the bacteria proliferated in the lungs. These data demonstrate that the cigarette smoke component, acrolein, not only depresses pulmonary bactericidal activity, but can also act as a stressor in aggravating an underlying disease process, resulting in an additional impairment of pulmonary antibacterial defenses.
|Original language||English (US)|
|Number of pages||6|
|Journal||American Review of Respiratory Disease|
|State||Published - Jan 1 1977|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine