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Viral mimic polyinosine-polycytidylic acid potentiates liver injury in trichloroethylene-sensitized mice – Viral-chemical interaction as a novel mechanism

Zhang, Cheng, Yu, Yun, Yu, Jun-feng, Li, Bo-dong, Zhou, Cheng-fan, Yang, Xiao-dong, Wang, Xian, Wu, Changhao, Shen, Tong and Zhu, Qi-xing (2018) Viral mimic polyinosine-polycytidylic acid potentiates liver injury in trichloroethylene-sensitized mice – Viral-chemical interaction as a novel mechanism Ecotoxicology and Environmental Safety, 155. pp. 101-108.

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Abstract

Occupational trichloroethylene (TCE) exposure can induce hypersensitivity dermatitis and severe liver injury. Recently, several clinical investigations indicate that viral infection, such as human herpesvirus-6, is associated with hepatic dysfunction in patients with TCE-related generalized skin disorders. However, whether viral infection potentiates TCE-induced liver injury remains unknown. This study aimed to explore the contribution of viral infection to the development of TCE-sensitization-induced liver injury in BALB/c mice. Female BALB/c mice were randomly assigned into four groups: solvent control group (n = 20), TCE group (n = 80), poly(I:C) group (n = 20) and combination of TCE and poly(I:C) (poly(I:C)+TCE) group (n = 80). Poly(I:C) (50 μg) was i.p. administrated. TCE and poly(I:C)+TCE groups were further divided into sensitization and non-sensitization subgroup. Complement 3 and C3a protein levels, and complement factors were measured. Combination treatment significantly enhanced TCE-induced liver injury, decreased complement 3, but increased C3a in serum and liver tissues in sensitization group. These changes were not correlated with the hepatic complement 3 transcription. Moreover, combination treatment specifically promoted complement factor B, but not factor D and factor H expressions. These data provide first evidence that poly(I:C) potentiates liver injury in BALB/c mouse model of TCE-sensitization. Upregulated C3a and factor B contributes to the poly(I:C) action in TCE-induced liver injury. This new mode of action may explain increased risk of chemical-sensitization induced tissue damage by viral infection.

Item Type: Article
Divisions : Faculty of Health and Medical Sciences > School of Biosciences and Medicine
Authors :
NameEmailORCID
Zhang, Cheng
Yu, Yun
Yu, Jun-feng
Li, Bo-dong
Zhou, Cheng-fan
Yang, Xiao-dong
Wang, Xian
Wu, ChanghaoC.Wu@surrey.ac.uk
Shen, Tong
Zhu, Qi-xing
Date : 3 March 2018
Funders : Biotechnology and Biological Sciences Research Council (BBSRC)
Identification Number : 10.1016/j.ecoenv.2018.02.056
Copyright Disclaimer : © 2018 Elsevier Inc. All rights reserved.
Uncontrolled Keywords : Trichloroethylene; Liver injury; Polyinosine-polycytidylic acid; Complement; Factor B
Depositing User : Clive Harris
Date Deposited : 13 Mar 2018 15:18
Last Modified : 13 Mar 2018 15:18
URI: http://epubs.surrey.ac.uk/id/eprint/845999

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