| First Author | Joe Y | Year | 2015 |
| Journal | Am J Pathol | Volume | 185 |
| Issue | 11 | Pages | 2867-74 |
| PubMed ID | 26348577 | Mgi Jnum | J:226904 |
| Mgi Id | MGI:5699188 | Doi | 10.1016/j.ajpath.2015.07.002 |
| Citation | Joe Y, et al. (2015) Tristetraprolin Mediates Anti-Inflammatory Effects of Carbon Monoxide on Lipopolysaccharide-Induced Acute Lung Injury. Am J Pathol 185(11):2867-74 |
| abstractText | 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. |
