AUTHOR=Zhan Tingzheng , Wu Yuhong , Deng Xueling , Li Qing , Chen Yu , Lv Jiahui , Wang Jilong , Li Shitao , Wu Zhanshuai , Liu Dengyu , Tang Zeli 

TITLE=Multi-omics approaches reveal the molecular mechanisms underlying the interaction between Clonorchis sinensis and mouse liver

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=Volume 13 - 2023

YEAR=2023

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2023.1286977

DOI=10.3389/fcimb.2023.1286977

ISSN=2235-2988

ABSTRACT=Clonorchiasis remains a serious global public health problem, causing various hepatobiliary diseases. However, there is still a lack of overall understanding regarding the molecular events induced by Clonorchis sinensis (C. sinensis) in the liver. The results of this study indicated unveil 删除[Zeli Tang]: its host 删除[Zeli Tang]: 删除[Zeli Tang]:that adult C. sinensis can cause systemic inflammation and liver damage. However, as the infection persisted, the Th2 immune response increased and symptoms were relieved.Multi-omics analysis of liver infected for 5 weeks identified 191, 402 and 232 differentially expressed genes (DEGs), proteins (DEPs) and metabolites (DEMs), respectively. Both DEGs and DEPs were significantly enriched in liver fibrosis-related pathways such as ECM-receptor interaction and cell adhesion molecules. Molecules associated with liver fibrosis or inflammation, including Cd34, Epcam, S100a6, Fhl2, Itgax, and Retnlg, were up-regulated at both the gene and protein levels. The top three metabolic pathways, namely purine metabolism, arachidonic acid metabolism, and ABC transporters, were associated with liver cirrhosis, fibrosis, and cholestasis, respectively. Metabolites that can promote liver inflammation and fibrosis, such as LysoPC(P-16:0/0:0), 20-COOH-leukotriene E4, and 14,15-DiHETrE, were significantly up-regulated. This study not only deepened our understanding of the progression of clonorchiasis but also provided insights into the molecular-level interaction mechanism between C. sinensis and its host liver.