Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock andsepsis. (Nat Med. 2013 Nov;19(11):1489-95.)

報告日期: 2015/05/15
報告時間: 16:00/16:50
報告學生: 王鍾漢
講評老師: 莊季瑛
附件下載: 下載[1491-1425859404-1.pdf] 

Cold-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock andsepsis.

Xiaoling Qiang, Weng-Lang Yang, Rongqian Wu, Mian Zhou, Asha Jacob,Weifeng Dong,Michael Kuncewitch, Youxin Ji, Huan Yang, Haichao Wang, Jun Fujita, Jeffrey Nicastro,Gene F Coppa, Kevin J Tracey and Ping Wang

Nature Medicine    2013, 19(11):1489-95.

Speaker:Chung-Han Wang                    Date:2015.5.15

Commentator:Jih-IngChuang               Location:Room 602

Abstract

World wide trauma is the leading cause of mortality. More than 6 million deaths occur due to trauma out of which 20% are due to uncontrollable bleeding. Hemorrhagic shock following major trauma results in a global ischemia and reperfusion injury that may lead to multiple organ dysfunction syndrome (MODS). Systemic activation of the immune system is fundamental to the development of MODS in this context, and shares many features in common with the systemic inflammatory response syndrome (SIRS) that complicates sepsis. Systemic inflammation can be triggered by exogenous pathogen-associated molecular pattern molecules (PAMPs) that are expressed on invading microorganisms during infection or by endogenous damage-associated molecular pattern molecules (DAMPs) that are released from host cells during tissue injury.Cold-inducible RNA-binding protein (CIRP) is a 172-amino acid nucleoprotein that belongs to the family of cold shock proteinsCold-inducible RNA-binding protein is originally identified to facilitate the translation by stabilizing mRNAs when cells are under certain stressful circumstances, including hypothermia, exposure to ultraviolet irradiation, or hypoxia.However, the expression of CIRP in human tissues has not been reported. In the study found CIRP in serum after hemorrhagic shock and sepsis , and identified that extracellular CIRP acts as a DAMP to accentuate the inflammatory response through binding to TLR4 and myeloid differentiation factor 2 (MD2) complex . Also, neutralizing antiserum to CIRP attenuates the inflammatory response in the settings of hemorrhagic shock and septic.

References

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