| Literature DB >> 26348577 |
Yeonsoo Joe1, Seul-Ki Kim1, Yingqing Chen1, Jung Wook Yang2, Jeong-Hee Lee2, Gyeong Jae Cho3, Jeong Woo Park4, Hun Taeg Chung5.
Abstract
Low-dose inhaled carbon monoxide is reported to suppress inflammatory responses and exhibit a therapeutic effect in models of lipopolysaccharide (LPS)-induced acute lung injury (ALI). However, the precise mechanism by which carbon monoxide confers protection against ALI is not clear. Tristetraprolin (TTP; official name ZFP36) exerts anti-inflammatory effects by enhancing decay of proinflammatory cytokine mRNAs. With the use of TTP knockout mice, we demonstrate here that the protection by carbon monoxide against LPS-induced ALI is mediated by TTP. Inhalation of carbon monoxide substantially increased the pulmonary expression of TTP. carbon monoxide markedly enhanced the decay of mRNA-encoding inflammatory cytokines, blocked the expression of inflammatory cytokines, and decreased tissue damage in LPS-treated lung tissue. Moreover, knockout of TTP abrogated the anti-inflammatory and tissue-protective effects of carbon monoxide in LPS-induced ALI. These results suggest that carbon monoxide-induced TTP mediates the protective effect of carbon monoxide against LPS-induced ALI by enhancing the decay of mRNA encoding proinflammatory cytokines.Entities:
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Year: 2015 PMID： 26348577 DOI： 10.1016/j.ajpath.2015.07.002
Source DB: PubMed Journal: Am J Pathol ISSN： 0002-9440 Impact factor: 4.307