| Literature DB >> 17030496 |
Helen M Marriott1, Paul G Hellewell, Moira K B Whyte, David H Dockrell.
Abstract
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 gp91(phox-/-) 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 gp91(phox-/-) mice. iNOS(-/-) mice recruit neutrophils and generate TNF-alpha to compensate for impaired AM competence but ROS deficiency has no apparent effect on AM function in this model.Entities:
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Year: 2006 PMID: 17030496 DOI: 10.1016/j.vaccine.2006.09.024
Source DB: PubMed Journal: Vaccine ISSN: 0264-410X Impact factor: 3.641