| Autor: |
Koay, M. Audrey, Christman, John W., Segal, Brahm H., Venkatakrishnan, Annapurna, Blackwell, Thomas R., Holland, Steven M., Blackwell, Timothy S. |
| Zdroj: |
Infection and Immunity; October 2001, Vol. 69 Issue: 10 p5991-5996, 6p |
| Abstrakt: |
ABSTRACTReactive oxygen species (ROS) are thought to be involved in intracellular signaling, including activation of the transcription factor NF-κB. We investigated the role of NADPH oxidase in the NF-κB activation pathway by utilizing knockout mice (p47phox−/−) lacking the p47phoxcomponent of NADPH oxidase. Wild-type (WT) controls and p47phox−/−mice were treated with intraperitoneal (i.p.) Escherichia colilipopolysaccharide (LPS) (5 or 20 μg/g of body weight). LPS-induced NF-κB binding activity and accumulation of RelA in nuclear protein extracts of lung tissue were markedly increased in WT compared to p47phox−/−mice 90 min after treatment with 20 but not 5 μg of i.p. LPS per g. In another model of lung inflammation, RelA nuclear translocation was reduced in p47phox−/−mice compared to WT mice following treatment with aerosolized LPS. In contrast to NF-κB activation in p47phox−/−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-κB activation is deficient in the lungs of p47phox−/−mice compared to WT mice, but this abnormality does not result in overt alteration in the acute inflammatory response. |
| Databáze: |
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