Effects of oxygen exposure on in vitro function of pulmonary alveolar macrophages.

Abstract

A B S T R A C T Bacterial infection may complicate pulmonary oxygen (02) toxicity, and animals exposed to high 02 concentrations show depressed in vivo pulmonary bacterial inactivation. Therefore, in vitro studies were undertaken to define the mechanism by which 02 alters pulmonary antibacterial activity. Normal and BCG pretreated rabbits were exposed to 100% 02 for 24, 48, and 72-h periods. Pulmonary alveolar macrophages (PAM) were obtained from the experimental animals and from nonoxygen exposed controls by bronchopulmonary lavage. 02 exposure did not alter cell yield or morphology. PAMs were suspended in 10% serum-buffer, and phagocytosis of ["C]Staphylococcus aureus 502A and ["C]Pseudomonas aeruginosa was measured. Comparison of the percent uptake of the "Clabeled S. aureus after a 60-min incubation period demonstrated that normal PAMs exposed to 02 for 48 h showed a statistically significant increase in phagocytosis when compared to their controls (43.5 vs. 29.2%). A similar, but smaller, increase was seen after 24-h 02 exposures. 48 and 72-h 02 exposures produced no significant changes in phagocytosis in PAMs from BCG-stimulated rabbits. Normal PAMs also showed an increased phagocytosis of Ps. aeruginosa after 48-h oxygen exposures. No impairment of in vitro bactericidal activity against either S. aureus 502A or Ps. aeruginosa could be demonstrated in PAMs from normal rabbits exposed to 02 for 48 h. These results indicate that the in vitro phagocytic and bactericidal capacity of the rabbit PAM is relatively resistant to the

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