Department of Medicine III, University Hospital, Aachen, Germany.
J Gastroenterol Hepatol. 2011 Mar;26(3):523-9. doi: 10.1111/j.1440-1746.2010.06436.x.
CXCL5 (chemokine [C-X-C motif] ligand 5, also known as epithelial neutrophil-activating peptide 78 [ENA78]) belongs to the CXC chemokine family and has been shown to have promitotic effects on hepatocytes. The aim of our study was to assess CXCL5 plasma levels in patients with chronic liver disease.
CXCL5 plasma levels were measured in 111 patients with chronic liver disease and 98 healthy controls. The gene expression of CXCL5 and its main receptor, CXC receptor-2, were also determined in liver biopsies from 46 patients.
CXCL5 levels were correlated with clinical presentation, laboratory parameters, and liver histology. Plasma CXCL5 levels in patients with liver cirrhosis were lower than those in healthy controls, and correlated with hepatic biosynthetic capacity, Child-Pugh and model for end-stage liver disease scores. Patients with hepatic necroinflammation and fibrosis on liver histology showed lower plasma CXCL5 levels. In patients with typical clinical complications of cirrhosis, CXCL5 levels were found to be decreased. Intrahepatically, CXCL5 expression was increased in patients with advanced fibrosis and cirrhosis. The isolation of different cellular compartments from mouse livers suggested that hepatic stellate cells and sinusoidal endothelial cells are the main sources of hepatic CXCL5.
Plasma CXCL5 levels are lower in patients with chronic liver disease, suggesting that CXCL5 might be involved in the pathogenesis of chronic liver disease. CXCL5 could serve as an additional biomarker for hepatic necroinflammation and fibrosis.
CXCL5(趋化因子[C-X-C 基序]配体 5,也称为上皮中性粒细胞激活肽 78[ENA78])属于 CXC 趋化因子家族,已被证明对肝细胞具有促有丝分裂作用。我们研究的目的是评估慢性肝病患者的 CXCL5 血浆水平。
测量了 111 例慢性肝病患者和 98 例健康对照者的 CXCL5 血浆水平。还在 46 例患者的肝活检中测定了 CXCL5 和其主要受体 CXC 受体-2 的基因表达。
CXCL5 水平与临床表现、实验室参数和肝组织学相关。肝硬化患者的血浆 CXCL5 水平低于健康对照组,与肝生物合成能力、Child-Pugh 和终末期肝病模型评分相关。肝组织学上有肝坏死炎症和纤维化的患者,其血浆 CXCL5 水平较低。在有肝硬化典型临床并发症的患者中,发现 CXCL5 水平降低。在纤维化和肝硬化患者中,肝内 CXCL5 表达增加。从小鼠肝脏中分离不同的细胞区室表明,肝星状细胞和窦内皮细胞是肝 CXCL5 的主要来源。
慢性肝病患者的血浆 CXCL5 水平较低,提示 CXCL5 可能参与慢性肝病的发病机制。CXCL5 可作为肝坏死炎症和纤维化的附加生物标志物。