Journal
INFECTION AND IMMUNITY
Volume 69, Issue 10, Pages 5991-5996Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.69.10.5991-5996.2001
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Funding
- NHLBI NIH HHS [R01 HL061419, HL 61419] Funding Source: Medline
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Reactive oxygen species (ROS) are thought to be involved in intracellular signaling, including activation of the transcription factor NF-kappaB. We investigated the role of NADPH oxidase in the NF-KB activation pathway by utilizing knockout mice (p47(phox-/-)) lacking the p47(phox) component of NADPH oxidase. Wild-type (WT) controls and P47(phox-/-) mice were treated with intraperitoneal (i.p.) Escherichia coli lipopolysaccharide (LPS) (5 or 20 mug/g of body weight). LPS-induced NF-kappaB binding activity and accumulation of RelA in nuclear protein extracts of lung tissue were markedly increased in WT compared to p47(phox-/-) mice 90 min after treatment with 20 but not 5 mug of i.p. LPS per g. In another model of lung inflammation, RelA nuclear translocation was reduced in p47(phox-/-) mice compared to. WT mice following treatment with aerosolized LPS. In contrast to NF-kappaB activation in p47(phox-/-) mice, LPS-induced production of macrophage inflammatory protein 2 in the lungs and neutrophilic lung inflammation were not diminished in these mice compared to WT mice. We conclude that LPS-induced NF-KB activation is deficient in the lungs of p47(phox-/-) mice compared to WT mice, but this abnormality does not result in overt alteration in the acute inflammatory response.
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