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- W242810705 abstract "Previous studies have shown that exposure of pathogen free C57BL/6N mice to 5 or 10 ppm of NO{sub 2} increased severity of murine respiratory mycoplasmosis and that this effect was associated with decreased intrapulmonary killing (IPK) of Mycoplasma pulmonis (MP). The purposes of the present studies were to titrate the NO{sub 2} effect and to determine if the changes in IPK were due to the effects of NO{sub 2} on alveolar macrophages. Exposure to less than 5 ppm NO{sub 2} had no effect on IPK of MP. Bronchoalveolar lavage (BAL) cells killed MP in vitro only if they were allowed to associate with mycoplasmas in vivo. Prior exposure to NO{sub 2} abrogated killing in this in vivo-in vitro model. Exposure to NO{sub 2} did not increase the protein content of BAL within 24 hours. Greater than 95% of the BAL cells were macrophages, and greater than 98% of the cell-associated mycoplasmas were on or in alveolar macrophages. Immediately after exposure, viability of alveolar macrophages, as measured by trypan blue exclusion and fluorescein diacetate uptake, was 89 {plus minus} 4% and 88 {plus minus} 4% in the control group, respectively; 56 {plus minus} 19% and 64 {plus minus} 11% in themore » group receiving MP alone; 23 {plus minus} 7% and 48 {plus minus} 9% in the group receiving 10 ppm NO{sub 2}; and 16 {plus minus} 6% and 25 {plus minus} 6% in the group receiving both MP and NO{sub 2} exposures. Viability was significantly decreased following exposure to 5 or 10 ppm NO{sub 2}, but not following exposure to 2 ppm. Viability did not return to normal until 7 days after exposure to NO{sub 2}, at which time IPK also returned to normal. The cellular target of NO{sub 2} exposure in relation to IPK of MP appears to be the alveolar macrophage.« less" @default.
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- W242810705 date "1991-03-11" @default.
- W242810705 modified "2023-09-23" @default.
- W242810705 title "Short term exposure to NO sup 2 decreases intrapulmonary killing of Mycoplasma pulmonis by damaging alveolar macrophages" @default.
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