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Title: Murine respiratory mycoplasmosis: a model to study effects of oxidants

Journal Article · · Research Report Health Effects Institue; (United States)
OSTI ID:5364231
; ;  [1]
  1. Department of Comparative Medicine, University of Alabama, Birmingham (United States)

Previous studies have shown that exposure to nitrogen dioxide at concentrations of 5 and 10 parts per million (ppm) decreases intrapulmonary killing of Mycoplasma pulmonis, and that this decrease is related to increased lung lesions and mortality. The specific objectives of the present study were to titrate the effects of nitrogen dioxide on pulmonary clearance of M. pulmonis, determine the mechanisms by which this organism is killed within the lungs, and determine the target that the nitrogen dioxide affects. Pathogen-free C57BL/6N mice were exposed to 0, 0.5, 1, 2, or 5 ppm of nitrogen dioxide (contamination with other oxides of nitrogen compounds was 5% or less) for four hours and then immediately were exposed to aerosols of viable, radiolabeled M. pulmonis strain UAB CT. One-half of the animals in each group were killed immediately after exposure to the infectious 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 nitrogen dioxide had no effect on intrapulmonary killing of M. pulmonis, although exposure to 1 ppm of nitrogen dioxide did increase mechanical removal. We were unable to develop a completely in vitro mycoplasma killing method. However, we were able to demonstrate the in vitro killing of M. pulmonis that had been allowed to associate with alveolar macrophages in vivo. Thus, mouse lungs contain unidentified factors that allow cells to kill M. pulmonis. Furthermore, we obtained evidence that suggests that prior exposure to nitrogen dioxide abrogates killing in these experiments. We also have shown that exposure to nitrogen dioxide does not increase the protein content of bronchoalveolar lavage fluid.

OSTI ID:
5364231
Journal Information:
Research Report Health Effects Institue; (United States), Vol. 47; ISSN 1041-5505
Country of Publication:
United States
Language:
English