NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, the First Affiliated Hospital, Shihezi University School of Medicine, Shihezi, Xinjiang, China.
Department of Immunology, Shihezi University School of Medicine, Shihezi, Xinjiang, China.
J Helminthol. 2023 Dec 21;97:e101. doi: 10.1017/S0022149X23000548.
Human cystic echinococcosis (CE) is a zoonotic disorder triggered by the larval stage of () and predominantly occurred in the liver and lungs. The M2 macrophage level is considerably elevated among the liver of patients with hepatic CE and performs an integral function in liver fibrosis. However, the mechanism of CE inducing polarisation of macrophage to an M2 phenotype is unknown. In this study, macrophage was treated with cyst fluid (EgCF) to explore the mechanism of macrophage polarisation. Consequently, the expression of the M2 macrophage and production of anti-inflammatory cytokines increased after 48 h treatment by EgCF. In addition, EgCF promoted polarisation of macrophage to an M2 phenotype by inhibiting the expression of transcriptional factor hypoxia-inducible factor 1-alpha (HIF-1α), which increased the expression of glycolysis-associated genes, including hexokinase 2 (HK2) and pyruvate kinase 2 (PKM2). The HIF-1α agonist ML228 also inhibited the induction of macrophage to an M2 phenotype by EgCF Our findings indicate that inhibits glycolysis by suppressing the expression of HIF-1α.
人类包虫病(CE)是一种由细粒棘球绦虫幼虫引起的人畜共患疾病,主要发生在肝脏和肺部。在肝泡型包虫病患者的肝脏中,M2 巨噬细胞水平显著升高,并在肝纤维化中发挥重要作用。然而,包虫诱导巨噬细胞向 M2 表型极化的机制尚不清楚。本研究用细粒棘球蚴囊液(EgCF)处理巨噬细胞,以探讨巨噬细胞极化的机制。结果表明,EgCF 处理 48 小时后,M2 巨噬细胞的表达和抗炎细胞因子的产生增加。此外,EgCF 通过抑制转录因子缺氧诱导因子 1 ɑ(HIF-1ɑ)的表达促进巨噬细胞向 M2 表型极化,从而增加糖酵解相关基因的表达,包括己糖激酶 2(HK2)和丙酮酸激酶 2(PKM2)。HIF-1ɑ激动剂 ML228 也抑制了 EgCF 诱导的巨噬细胞向 M2 表型的诱导。我们的研究结果表明,EgCF 通过抑制 HIF-1ɑ的表达抑制糖酵解。