State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
College of Basic Medicine of Xinjiang Medical University, Urumqi, China.
Front Cell Infect Microbiol. 2020 Jan 29;10:8. doi: 10.3389/fcimb.2020.00008. eCollection 2020.
Kupffer cells (KCs) are the liver-resident macrophages and play a leading role in the regulation of liver homeostasis in physiological conditions and in pathology. The study aims to investigate the anti-echinococcosis effect of KCs and the effects of hepatic stellate cells (HSCs) activation in the progression of liver fibrosis in hepatic alveolar echinococcosis (hepatic AE). Hematoxylin-eosin (H&E) and Masson staining were used to assess the pathological inflammatory changes and collagen deposition, respectively. Immunohistochemistry and qRT-PCR were used to detect the number of aggregates of KCs, the expression of cytokines and activation of HSCs. In the close group, H&E staining showed that the normal lobular structure was destroyed and inflammatory infiltration around the lesion could be observed, and Masson staining showed that blue collagen fibers were clearly deposited near the portal area. IHC showed that KCs surface markers CD68 and CD163, cytokine iNOS and Arg-1 were positively expressed in the vicinity of inflammatory lesions. qRT-PCR indicated that TNF-α, IL-10, and TGF-β1 secreted by KCs were significantly higher than those in the distance group ( < 0.01). It is worth noticing that the expression levels of anti-inflammatory cytokines were slightly higher than that of pro-inflammatory cytokines. Both IHC and qRT-PCR results showed that HSCs activation markers, the expression of α-SMA and Desmin significantly increased. Our research indicates that KCs have immune-protective effect of anti-echinococcosis and promote liver fiber repair, and it also suggests that they have potential therapeutic value for patients with hepatic AE.
枯否细胞(KCs)是肝脏驻留的巨噬细胞,在生理条件下和病理学中,在调节肝脏内稳态方面发挥主导作用。本研究旨在探讨 KCs 在肝泡状棘球蚴病(hepatic AE)肝纤维化进展中的抗包虫病作用以及肝星状细胞(HSCs)激活的影响。苏木精-伊红(H&E)和 Masson 染色分别用于评估病理性炎症变化和胶原沉积。免疫组织化学和 qRT-PCR 用于检测 KCs 聚集的数量、细胞因子的表达和 HSCs 的激活。在紧密组中,H&E 染色显示正常小叶结构被破坏,病变周围可观察到炎症浸润,Masson 染色显示蓝色胶原纤维在门脉区附近明显沉积。免疫组化显示 KCs 表面标志物 CD68 和 CD163、细胞因子 iNOS 和 Arg-1 在炎症病灶附近呈阳性表达。qRT-PCR 表明 KCs 分泌的 TNF-α、IL-10 和 TGF-β1 明显高于远隔组(<0.01)。值得注意的是,抗炎细胞因子的表达水平略高于促炎细胞因子。免疫组化和 qRT-PCR 结果均显示 HSCs 激活标志物α-SMA 和 Desmin 的表达明显增加。我们的研究表明 KCs 具有抗包虫病的免疫保护作用,并促进肝纤维修复,这也表明它们对肝泡状棘球蚴病患者具有潜在的治疗价值。