| First Author | Yang Y | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 480 |
| Issue | 3 | Pages | 486-491 |
| PubMed ID | 27780729 | Mgi Jnum | J:240806 |
| Mgi Id | MGI:5896461 | Doi | 10.1016/j.bbrc.2016.10.080 |
| Citation | Yang Y, et al. (2016) Looped limulus anti-lipopolysaccharide derived peptide CLP-19 induces endotoxin tolerance involved inhibition of NF-kappaB activation. Biochem Biophys Res Commun 480(3):486-491 |
| abstractText | Endotoxin tolerance (ET) is a complex protective mechanism against endotoxin shock. The looped CLP-19 peptide derived from Limulus anti-LPS peptide induced the ET phenomenon but the molecular mechanism has yet to be fully elucidated. Here, we confirmed that CLP-19 attenuated upon LPS stimulated pro-inflammatory factor secretion of TNF-alpha and IL-6 but increased anti-inflammatory factor production of IL-10 in dose- and time-dependent manners. CLP-19 also inhibited subsequent LPS stimulated expression of TLR4 on the cell membrane. Moreover, the CLP-19 inhibited degradation of the inhibitor of NF-kappaB (IkappaBalpha and IkappaBbeta) and reduced LPS induced NF-kappaB activity, but not of effects on expression of MyD88 and TRAF-6. Finally CLP-19 significantly increased survival of lethal LPS shock mouse models with significantly less pathological injury to lung. These findings collectively suggest that CLP-19 induces ET phenomenon involved inhibition of NF-kappaB activation. In conclusion, this study has revealed a novel function of CLP-19 that appears to represent a potential therapeutic agent for clinical treatment of septic shock. |
