Abstract
Aims: 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).Methods: 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.Results: 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 (P < 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.Conclusions: 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.
Highlights
Alveolar echinococcosis (AE), caused by Echinococcus multilocularis. is characterized by a large multilocular cyst with a jelly-like substance, instead of clear hydatid fluid
It is estimated that nearly 2 billion people worldwide are infected with worms (Hotez et al, 2008) and about 200 million cases are echinococcosis, of which, 0.3% are caused by AE (Craig et al, 2017)
The main purpose of this study is to investigate the antialveolar echinococcosis effect of Kupffer cells (KCs) in hepatic AE accompanied with liver fibrosis, and aims to evaluate KCs’ potential therapeutic value in the treatment of liver fibrosis caused by persistent AE infection
Summary
Alveolar echinococcosis (AE), caused by Echinococcus multilocularis. is characterized by a large multilocular cyst with a jelly-like substance, instead of clear hydatid fluid. Cysts localize first in the liver, and in the early stages, the infection is generally asymptomatic (Arrechea Irigoyen et al, 2008). Such classification is a necessary tool when making therapeutic decisions for the treatment of this disease (Kern et al, 2006). AE is a serious lifethreatening chronic helminthiasis caused by E. multilocularis. It mostly occurs in the liver and is known to be slowly progressive but often, a fatal disease. It is estimated that nearly 2 billion people worldwide are infected with worms (Hotez et al, 2008) and about 200 million cases are echinococcosis, of which, 0.3% are caused by AE (Craig et al, 2017). The variability and severity of the clinical manifestations of this parasitic disease are related to the duration and degree of infection (Mezioug and Touil-Boukoffa, 2012)
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