Short-term Exposure to Nitrogen Dioxide Enhances Susceptibility to Murine Respiratory Mycoplasmosis and Decreases Intrapulmonary Killing ofMycoplasma pulmonis

Abstract

In C57BL/6N and C3H/HeN mice known to be free of all murine pathogens and matched for age, sex, microbiologic, and environmental factors, exposure to NO2 for 4 h prior to exposure to infectious aerosols of Mycoplasma pulmonis resulted in potentiation of murine respiratory mycoplasmosis (MRM). In the C57BL/6N mice, NO2 increased the incidence of death, incidence of gross lung lesions, and incidence of microscopic lung lesions, but did not increase the incidence of infection in the lungs. Nitrogen dioxide affected the C3H/HeN mice (a strain known to be more susceptible than the C57BL/6N strain to MRM) similarly, with the exception that the incidence of death and microscopic lesions were not affected in this strain at the concentrations of M. pulmonis used. Exposure to the oxidant also increased the severity of microscopic lesions and the numbers of Mycoplasma organisms in the lungs of both mouse strains. Thus, NO2 appeared to affect host lung defense mechanisms responsible for limiting the extent of infection. The NO2 exposure level required to produce potentiation varied with the genetic background of the host, the number of Mycoplasma organisms administered, and the end point measured. In further experiments in C57BL/6N mice, exposure to 5 or 10 ppm of NO2 for 4 h prior to infection with aerosolized, radiolabeled M. pulmonis reduced clearance of these organisms from the lungs over a 72-h time period. Nitrogen dioxide exposure did not change the rate of physical removal of Mycoplasma organisms from the lung. Reduced clearance was due to impaired intrapulmonary killing of Mycoplasma organisms in NO2-exposed mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic respiratory mycoplasmosis in C3H/HeN and C57BL/6N mice: lesion severity and antibody response

“…In contrast, C57BL/6N mice had equivalent or more severe epithelial and lymphoid hyperplasia in nasal passages. This is similar to results described for acute disease in mice where the difference in disease was associated with nonspecific clearance of organisms (25). Thus, C3H/HeN and C57BL/6N mice differed in the severity of chronic MRM in the lower, but not the upper, respiratory tract after infection with M. pulmonis.…”

T lymphocyte responses are critical determinants in the pathogenesis and resistance to mycoplasma respiratory disease

“…Our recent studies demonstrate that male mice develop more severe alveolar pneumonia after M. pulmonis infection (29), which is consistent with disease due to the human mycoplasma, M. pneumonia (5,6,30). In addition to host factors, environmental factors, such as the levels of ammonia and pollutants, also impact on mycoplasma respiratory diseases (31,32). However, the effects of the environmental factors are most likely on the host, particularly defense mechanisms.…”

Gaseous Air Pollutants and Hospitalization for Respiratory Disease in the Neonatal Period

“…Controlled human exposures to NO 2 have demonstrated small increases in bronchial reactivity (Folinsbee 1992) and an enhanced effect of allergen-induced bronchoconstriction (Strand et al 1998). In mice, NO 2 exposure increases morbidity from Mycoplasma pulmonis (Parker et al 1989) and mortality from Klebsiella Pneumoniae (Ehrlich 1966; Gauderman et al 2000; Peters et al 1999a, 1999b; Stieb et al 2002). The effects of NO 2 in large observational studies have been found at lower concentrations than those investigated in laboratory studies.…”