Murine Respiratory Mycoplasmosis: A Model to Study Effects of Oxidants.

摘要

Pathogen-free mice were exposed to 0, 0.5, 1, 2, or 5 parts per million of nitrogen dioxide and then to aerosols of radiolabeled Mycoplasma pulmonis. One-half of the animals in each group were killed immediately after exposure to the aerosols, and the rest were killed 24 hours later. The amount of radioactivity and the number of viable M. pulmonis were determined for each group. Exposure to less than 5 ppm of NO2 had no effect on intrapulmonary killing of M. pulmonis. The authors demonstrated in vitro killing of M. pulmonis that were associated with alveolar macrophages in vivo. Thus, mouse lungs contain unidentified factors that allow cells to kill M. pulmonis. Their evidence suggests that prior exposure to nitrogen dioxide abrogates killing. More than 95% of the cells recovered by lavage were macrophages. More than 98% of the cell-associated mycoplasmas were on or in alveolar macrophages. In lung lavage cells from mice exposed to NO2, M. pulmonis, or both, each insult affected the viability of recovered macrophages. Significant effects on macrophage viability were seen after exposure to 5 and 10 ppm NO2, but not after exposure to 2 ppm. Macrophage viability in the groups exposed to NO2 did not completely return to normal until seven days after exposure, when intrapulmonary killing also returned to normal. The effect of NO2 exposure in relation to intrapulmonary killing of M. pulmonis appears to be decreased alveolar macrophage function.