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 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.
Marriott
Helen M
HM
School of Medicine and Biomedical Sciences, L-Floor, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK.
Hellewell
Paul G
PG
Whyte
Moira K B
MK
Dockrell
David H
DH
D000818:Animals; D017209:Apoptosis / Q000276:immunology; D005260:Female; D007113:Immunity, Innate / Q000276:immunology; D008168:Lung / Q000382:microbiology*; D016676:Macrophages, Alveolar / Q000276:immunology* / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000172:deficiency; D051379:Mice; D008810:Mice, Inbred C57BL; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases / Q000172:deficiency; D009569:Nitric Oxide / Q000276:immunology* / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000172:deficiency; D011008:Pneumococcal Infections / Q000276:immunology* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000276:immunology* / Q000378:metabolism; D013296:Streptococcus pneumoniae / Q000276:immunology* / Q000378:metabolism
D008562:Membrane Glycoproteins; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C488842:Cybb protein, mouse; D000074662:NADPH Oxidase 2; D019255:NADPH Oxidases