Abstract
BackgroundSchistosoma japonicum is a parasitic flatworm that is the aetiological agent of human schistosomiasis, an important cause of hepatic fibrosis. Schistosomiasis-induced hepatic fibrosis is a consequence of the highly fibrogenic nature of egg-induced granulomatous lesions, which are the main pathogenic features of schistosomiasis. Although global awareness of the association between schistosomiasis-induced hepatic fibrosis and S. japonicum infection is increasing, little is known about the molecular differences associated with rapid progression to schistosomiasis in cirrhotic patients.MethodsWe systematically used data-independent acquisition (DIA)-based liquid chromatography-mass spectrometry to identify differentially expressed proteins in serum samples from patients with advanced S. japonicum-induced hepatic fibrosis.ResultsOur analysis identified 1144 proteins, among which 66 were differentially expressed between the healthy control group and the group of patients with advanced S. japonicum-induced hepatic fibrosis stage F2 (SHF-F2) and 214 were differentially expressed between the SHF-F2 and SHF-F4 groups (up- or downregulation of at least 1.5-fold in serum samples). The results also indicated that two selected proteins (C1QA and CFD) are potential biomarkers for distinguishing between patients with SHF-F2 and those with SHF-F4 due to S. japonicum infection.ConclusionsWe provide here the first global proteomic profile of serum samples from patients with advanced S. japonicum-induced hepatic fibrosis. The proteins C1QA and CFD are potential diagnostic markers for patients with SHF-F2 and SHF-F4 due to S. japonicum infection, although further large-scale studies are needed. Our DIA-based quantitative proteomic analysis revealed molecular differences among individuals at different stages of advanced S. japonicum-induced hepatic fibrosis and may provide fundamental information for further detailed investigations.Graphical
Highlights
Schistosoma japonicum is a parasitic flatworm that is the aetiological agent of human schistosomiasis, an important cause of hepatic fibrosis
S. japonicum is the major species causing schistosomiasis in Southeast Asia, including China, and is associated with severe pathogenicity induced by the eggs of adult worms and subsequent schistosomiasis-induced hepatic fibrosis (SHF) that eventually develops into hepatocellular carcinoma (HCC), which is the main cause of schistosomiasis-related mortality [2, 5,6,7]
alkaline phosphatase (ALP) Alkaline phosphatase, ALT alanine aminotransferase, APRI AST-to-PLT ratio index, APTT activated partial thromboplastin, AST aspartate aminotransferase, FIB fibrinogen content, GGTgamma-glutamyltranspeptidase, INR international normalized ratio, N/A information not available, PLT platelet count, SHF schistosomiasisinduced hepatic fibrosis, PT prothrombin time, TB total bilirubin, TBA total bile acid *P value < 0.05 for comparisons between patients with SHF stage F2 and healthy controls, and §P value < 0.05 for comparisons between patients with SHF stage F4 and and those with SHF stage F2. a SHF was staged from F0 to F4 according the METAVIR scoring system b Student’s t-test for comparisons between patients with SHF stage F2 and healthy controls c Student’s t-test for comparisons between patients with SHF stage F4 and those with SHF stage F2
Summary
Schistosoma japonicum is a parasitic flatworm that is the aetiological agent of human schistosomiasis, an important cause of hepatic fibrosis. Schistosomiasis, called bilharzia, is the second most prevalent parasitic disease worldwide It is caused by blood flukes (trematode worms) of the genus Schistosoma and annually over 229 million people worldwide. S. japonicum is the major species causing schistosomiasis in Southeast Asia, including China, and is associated with severe pathogenicity induced by the eggs of adult worms and subsequent schistosomiasis-induced hepatic fibrosis (SHF) that eventually develops into HCC, which is the main cause of schistosomiasis-related mortality [2, 5,6,7]. Over time and/or with repeated or long-term infection, these granulomas, which develop at the sites of maximal egg accumulation, progress to severe and often irreversible SHF that disrupts hepatic blood flow, in turn obstructs portal venous flow and may lead to potentially life-threatening variceal bleeding [7, 12,13,14]. The factors that can prevent this complication from developing remain poorly understood [3]
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