Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 4, Pages 2622-2629Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.4.2622
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Funding
- NHLBI NIH HHS [R01HL60234, R01HL55330] Funding Source: Medline
- NIAID NIH HHS [R01AI42365] Funding Source: Medline
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Carbon monoxide (CO), a product of heme oxygenase activity, exerts antiapoptotic and anti-inflammatory effects in vitro and in vivo. The anti-inflammatory effects of CO involve the inhibition of TNF-alpha expression and the enhancement of IL-10 production, resulting in reduced mortality after endotoxin challenge. In this study we demonstrate for the first time that the protective effects of CO involve the increased expression of the 70-kDa inducible beat shock protein (Hsp70) in murine lung endothelial cells and fibroblasts. The p38 beta MAPK mediated the effects of CO on cytoprotection and Hsp70 regulation. Suppression of Hsp70 expression and/or genetic deletion of heat shock factor-1, the principle transcriptional regulator of Hsp70, attenuated the cytoprotective and immunomodulatory effects of CO in mouse lung cells and in vivo. These data provide a novel mechanism for the protective effects of CO and underscore a potential application of this gaseous molecule in anti-inflammatory therapies.
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