The acute phase C-reactive protein (CRP) is mainly synthesized and secreted by the liver in a cytokine-mediated response to infection or inflammation and circulates as a pentamer (pCRP) in plasma. Recent studies indicate that CRP is not only a marker but is directly involved in inflammation. CRP has a vital role in host defense and inflammation, metabolic function and scavenging through its ability for calcium depended binding to exogenous and endogenous molecules having phosphocholine followed by activation of the classical complement pathway. Accumulating evidence indicates that pCRP dissociates into monomeric CRP (mCRP) and most proinflammatory actions of CRP are only expressed following dissociation of its native pentameric assembly into mCRP. The dissociation of CRP into mCRP altogether promotes the ligand-binding capability. mCRP emerges to be the main conformation of CRP that participates in the regulation of local inflammation, however, little is identified concerning what triggers the significantly enhanced actions of mCRP and their binding to diverse ligands. The separation of mCRP from pCRP may be a direct relationship between CRP and inflammation. Here we review the current literature on CRP dissociation and its interaction with different ligands. The possibility to avoid the generation of the proinflammatory potential of mCRP has driven therapeutic approaches by targeting the dissociation mechanism of pCRP or inhibition of mCRP itself during inflammation.

急性期 C 反应蛋白 (CRP) 主要由肝脏在细胞因子介导的感染或炎症反应中合成和分泌，并作为五聚体 (pCRP) 在血浆中循环。最近的研究表明，CRP 不仅是一种标志物，而且直接参与炎症。CRP 通过其与具有磷酸胆碱的外源性和内源性分子结合的能力，随后激活经典补体途径，在宿主防御和炎症、代谢功能和清除中具有重要作用。越来越多的证据表明 pCRP 解离为单体 CRP (mCRP)，并且 CRP 的大多数促炎作用仅在其天然五聚体组装解离为 mCRP 后才表达。CRP 解离成 mCRP 完全促进了配体结合能力。mCRP 成为参与局部炎症调节的 CRP 的主要构象，然而，关于是什么触发了 mCRP 显着增强的作用及其与多种配体的结合，目前尚不清楚。mCRP 与 pCRP 的分离可能是 CRP 与炎症之间的直接关系。在这里，我们回顾了当前关于 CRP 解离及其与不同配体相互作用的文献。避免产生 mCRP 促炎潜能的可能性通过靶向 pCRP 的解离机制或在炎症期间抑制 mCRP 本身推动了治疗方法。关于是什么触发了 mCRP 显着增强的作用及其与不同配体的结合，几乎没有发现。mCRP 与 pCRP 的分离可能是 CRP 与炎症之间的直接关系。在这里，我们回顾了当前关于 CRP 解离及其与不同配体相互作用的文献。避免产生 mCRP 促炎潜能的可能性通过靶向 pCRP 的解离机制或在炎症期间抑制 mCRP 本身推动了治疗方法。关于是什么触发了 mCRP 显着增强的作用及其与不同配体的结合，几乎没有发现。mCRP 与 pCRP 的分离可能是 CRP 与炎症之间的直接关系。在这里，我们回顾了当前关于 CRP 解离及其与不同配体相互作用的文献。避免产生 mCRP 促炎潜能的可能性通过靶向 pCRP 的解离机制或在炎症期间抑制 mCRP 本身推动了治疗方法。