Interleukin-33 deficiency prevents biliary injuries and repairments caused by Clonorchis sinensis via restraining type 2 cytokines

Autor: Chao Yan, Na Xu, Man Liu, Zhihua Jiang, Jing Wu, Stephane Koda, Yu Chen, Beibei Zhang, Qian Yu, Yin-Hai Xu, Jian-Lin Wu, Kui-Yang Zheng
Jazyk: angličtina
Rok vydání: 2022
Předmět:
Zdroj: Parasites & Vectors, Vol 15, Iss 1, Pp 1-9 (2022)
Druh dokumentu: article
ISSN: 1756-3305
DOI: 10.1186/s13071-022-05490-6
Popis: 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
Databáze: Directory of Open Access Journals