INSERM U895, Team 8 Hepatic Complications of Obesity, Nice, France.
PLoS One. 2010 Oct 22;5(10):e13577. doi: 10.1371/journal.pone.0013577.
Obesity modulates inflammation and activation of immune pathways which can lead to liver complications. We aimed at identifying expression patterns of inflammatory and immune response genes specifically associated with obesity and NASH in the liver of morbidly obese patients.
METHODOLOGY/PRINCIPAL FINDINGS: Expression of 222 genes was evaluated by quantitative RT-PCR in the liver of morbidly obese patients with histologically normal liver (n = 6), or with severe steatosis without (n = 6) or with NASH (n = 6), and in lean controls (n = 5). Hepatic expression of 58 out of 222 inflammatory and immune response genes was upregulated in NASH patients. The most notable changes occurred in genes encoding chemokines and chemokine receptors involved in leukocyte recruitment, CD and cytokines involved in the T cell activation towards a Th1 phenotype, and immune semaphorins. This regulation seems to be specific for the liver since visceral adipose tissue expression and serum levels of MCP1, IP10, TNFα and IL6 were not modified. Importantly, 47 other genes were already upregulated in histologically normal liver (e.g. CRP, Toll-like receptor (TLR) pathway). Interestingly, serum palmitate, known to activate the TLR pathway, was increased with steatosis.
CONCLUSION/SIGNIFICANCE: The liver of obese patients without histological abnormalities already displayed a low-grade inflammation and could be more responsive to activators of the TLR pathway. NASH was then characterized by a specific gene signature. These findings help to identify new potential actors of the pathogenesis of NAFLD.
肥胖会调节炎症和免疫途径的激活,从而导致肝脏并发症。我们旨在确定与肥胖和 NASH 相关的炎症和免疫反应基因在病态肥胖患者肝脏中的表达模式。
方法/主要发现:通过定量 RT-PCR 评估 222 个基因在组织学正常的病态肥胖患者肝脏(n=6)、无 NASH 的严重脂肪变性(n=6)或有 NASH 的病态肥胖患者肝脏(n=6)和瘦对照组(n=5)中的表达。在 NASH 患者中,58 个炎症和免疫反应基因中有 58 个在肝脏中上调。最显著的变化发生在编码趋化因子和趋化因子受体的基因中,这些基因参与白细胞募集、CD 和细胞因子参与 T 细胞向 Th1 表型的激活,以及免疫信号素。这种调节似乎是肝脏特有的,因为内脏脂肪组织表达和 MCP1、IP10、TNFα 和 IL6 的血清水平没有改变。重要的是,47 个其他基因在组织学正常的肝脏中已经上调(例如 CRP、Toll 样受体(TLR)途径)。有趣的是,已知激活 TLR 途径的血清棕榈酸在脂肪变性时增加。
结论/意义:没有组织学异常的肥胖患者的肝脏已经显示出低度炎症,并且可能对 TLR 途径的激活剂更敏感。NASH 的特征是特定的基因特征。这些发现有助于确定非酒精性脂肪性肝病发病机制的新潜在因素。