Oliviero Francesca, Scanu Anna
Rheumatology Unit, Department of Medicine - DIMED, University of Padova Padova, Italy.
Front Pharmacol. 2017 Mar 28;8:164. doi: 10.3389/fphar.2017.00164. eCollection 2017.
One of the main clinical features characterizing crystal-induced inflammation is its spontaneous resolution. The aim of this review is to outline the various factors involved in the self-limiting course of crystal-induced inflammation focusing on their effect on IL-1β production. Endogenous molecules that are induced or locally recruited by the process itself, inhibitory proteins naturally present in the joint and exogenous dietary factors are discussed. Aside from the classical well-known molecules involved in the resolution of crystal-induced acute attack such as TGFβ, IL-10, IL-1Ra, and lipoproteins, particular attention is paid to recently uncovered mechanisms such as the aggregation of neutrophil extracellular traps, the release of ectosomes from neutrophil surface, and alpha-1-anti-trypsin-mediated IL-1 inhibition.
晶体诱导性炎症的主要临床特征之一是其可自发消退。本综述的目的是概述晶体诱导性炎症自限过程中涉及的各种因素,重点关注它们对白细胞介素-1β(IL-1β)产生的影响。文中讨论了由该过程本身诱导或局部募集的内源性分子、关节中天然存在的抑制性蛋白以及外源性饮食因素。除了参与晶体诱导性急性发作消退的经典知名分子,如转化生长因子β(TGFβ)、白细胞介素-10(IL-10)、白细胞介素-1受体拮抗剂(IL-1Ra)和脂蛋白外,还特别关注了最近发现的机制,如中性粒细胞胞外陷阱的聚集、中性粒细胞表面外泌体的释放以及α-1抗胰蛋白酶介导的IL-1抑制。