目的：Chemerin是一个强有力的趋化因子,在慢性胰腺炎炎症和免疫过程中发挥重要的作用。检测慢性胰腺炎患者血清chemerin浓度，可以通过增加纤维化细胞因子的产生进而影响慢性胰腺炎进程的假设。方法：用ELISA法测定男性酒精性胰腺炎患者（40个非糖尿病患者和28个糖尿病患者）血清chemerin 浓度和导致胰腺纤维化的细胞因子如血小板衍生生长因子BB和转化生长因子β-1，用40岁健康人做对照。结果：血清Chemerin同时在非糖尿病和糖尿病的慢性胰腺炎患者与对照组相比增加。此外，慢性胰腺炎患者血清chemerin和血小板衍生生长因子BB以及转化生长因子β-1浓度之间呈正相关。结论：结果表明：（1）慢性胰腺炎血清chemerin浓度增加。（2）血清chemerin浓度和主要纤维化细胞因子的血清浓度相关。Chemerin水平升高，刺激巨噬细胞浸润胰腺，可能会导致生产过剩的血小板衍生生长因子BB和转化生长因子β-1，导致胰腺纤维化。
吉林大学第一医院肝胆胰内科 何芳慧 摘译
本文首次发表于[Dig Liver Dis. 2012;44(5):393-397]
Increased serum chemerin concentration in patients with chronic pancreatitis
Abstract
BACKGROUND AND AIMS: Chemerin is a potent chemoattractant expressing cells and is involved in inflammatory and immune processes that play an important role in chronic pancreatitis.To test the hypothesis that serum chemerin concentration may be affected in chronic pancreatitis patients and that chemerin can influence the course of chronic pancreatitis by increasing profibrotic cytokine production.
METHODS:Serum concentrations of chemerin and the major cytokines involved in pancreatic fibrosis such as platelet-derived growth factor BB and TGF β-1 were determined by ELISA in samples from 40 nondiabetic and 28 diabetic male patients with chronic pancreatitis of alcoholic origin and 40 age-matched healthy controls.
RESULTS:Serum concentrations of chemerin were increased both in nondiabetic and diabetic chronic pancreatitis patients compared to controls. Moreover, in chronic pancreatitis patients a positive correlation was found between serum chemerin and platelet-derived growth factor BB as well as transforming growth factor β-1 concentrations.
CONCLUSIONS:The results indicate that: (a) chronic pancreatitis in humans is associated with an increased serum chemerin concentration and (b) serum chemerin concentration correlates with serum concentrations of the major profibrotic cytokines. Elevated level of chemerin, by stimulating macrophage infiltration of the pancreas, might lead to overproduction of platelet-derived growth factor BB and transforming growth factor β-1 and, consequently, to pancreatic fibrosis.
