Contrasting roles for reactive oxygen species and nitric oxide in the innate response to pulmonary infection with Streptococcus pneumoniae

The pulmonary innate response to low-dose bacterial challenge requires functioning alveolar macrophages (AM) but also subsequent macrophage apoptosis. To address the role of reactive oxygen species (ROS) and nitric oxide (NO) in AM apoptosis, sub-clinical Streptococcus pneumoniae infection was established in gp91phox−/− and inducible NO synthase deficient (iNOS−/−) mice. Both AM apoptosis and the number of macrophages containing apoptotic bodies are reduced in iNOS−/− as compared to control or gp91phox−/− mice. iNOS−/− mice recruit neutrophils and generate TNF-α to compensate for impaired AM competence but ROS deficiency has no apparent effect on AM function in this model.