10.6084/M9.FIGSHARE.C.6261482.V1
Chao Yan
Chao
Yan
Xuzhou Medical College
Na Xu
Na
Xu
Xuzhou Medical College
Man Liu
Man
Liu
Xuzhou Medical College
Zhihua Jiang
Zhihua
Jiang
Guangxi Center for Disease Prevention and Control
Jing Wu
Jing
Wu
Xuzhou Medical College
Stephane Koda
Stephane
Koda
Xuzhou Medical College
Yu Chen
Yu
Chen
Nanning Center for Disease Control and Prevention
Beibei Zhang
Beibei
Zhang
Xuzhou Medical College
Qian Yu
Qian
Yu
Xuzhou Medical College
Yin-Hai Xu
Yin-Hai
Xu
Affiliated Hospital of Xuzhou Medical College
Jian-Lin Wu
Jian-Lin
Wu
Guangxi Medical University
Kui-Yang Zheng
Kui-Yang
Zheng
Xuzhou Medical College
Interleukin-33 deficiency prevents biliary injuries and repairments caused by Clonorchis sinensis via restraining type 2 cytokines
Abstract Background Clonorchiasis caused by Clonorchis sinensis is a zoonotic parasitic disease characterized by cholangitis, biliary proliferation, biliary fibrosis, and even cholangiocarcinoma. Our previous study showed that the expression of interleukin (IL)-33 is increased in both humans and mice infected by C. sinensis, suggesting that IL-33 is potentially involved in the pathogenesis of clonorchiasis. However, the roles and potential mechanism of IL-33 underlying remain unknown. Methods Wild-type (WT) and IL-33 knockout (KO) mice (BALB/c female mice) were orally infected with 45 metacercariae of C. sinensis for 8 weeks. Biliary injuries and fibrosis were extensively evaluated. Hepatic type II cytokines (IL-4, IL-13, and IL-10) were detected by ELISA. Results For wild-type mice, we found that the mice infected with C. sinensis showed severe biliary injuries and fibrosis compared with the normal mice that were free from worm infection. In addition, the levels of type II cytokines such as IL-4, IL-13, and IL-10 in infected wild-type mice were significantly higher than in the control mice without infection (P < 0.05). However, IL-33 deficiency (IL-33 KO) prevents the augmentation of biliary injuries and fibrosis caused by C. sinensis infection. Furthermore, the increased levels of these type II cytokines induced by worm infection were also reversed in IL-33 KO mice. Conclusion Our present study demonstrates that IL-33 contributes to the pathogenesis of C. sinensis-induced biliary injuries and repair, which can potentially orchestrate type 2 responses. These findings highlight the pathophysiological role of IL-33 in the progression of clonorchiasis.
Biochemistry
Medicine
Microbiology
Molecular Biology
Science Policy
Immunology
Biological Sciences not elsewhere classified
Computational Biology
figshare
2022
2022-10-22
2022-10-22
Collection
10.6084/m9.figshare.c.6261482
CC BY 4.0