Inhaled fluticasone propionate reduces concentration of Mycoplasma pneumoniae, inflammation, and bronchial hyperresponsiveness in lungs of mice.

BACKGROUND: Mycoplasma pneumoniae has been shown to induce airway inflammation and bronchial hyperresponsiveness (BHR) in mice. Inhaled corticosteroids are the mainstay of asthma treatment, but their effects on M. pneumoniae and associated airway inflammation and BHR are poorly understood.
METHODS: Four groups of mice were studied to determine whether inhaled fluticasone propionate (FP) could attenuate airway inflammation and BHR by reducing or eliminating M. pneumoniae in lungs. The active group received aerosolized FP once daily for 5 days. Control mice received aerosolized sham solution plus M. pneumoniae, sham solution alone, or FP alone.
RESULTS: Mice treated with sham solution or FP alone did not develop airway inflammation or BHR. Mice infected with M. pneumoniae (no FP) developed significant lung inflammation and BHR. FP treatment of infected mice reduced neutrophils in bronchoalveolar lavage fluid (BALF), lung inflammation, and BHR. Expression of Toll-like receptor 2 in lung tissue tended to be down-regulated (P=.18) by FP in infected mice. FP reduced M. pneumoniae by up to 20-fold in lung tissue but not in BALF.
CONCLUSION: Inhaled FP suppresses airway inflammation and BHR, which may be caused, in part, by its ability to reduce concentrations of M. pneumoniae in lung tissue.