Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8854022 | Ecotoxicology and Environmental Safety | 2018 | 8 Pages |
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 (nâ¯=â¯20), TCE group (nâ¯=â¯80), poly(I:C) group (nâ¯=â¯20) and combination of TCE and poly(I:C) (poly(I:C)+TCE) group (nâ¯=â¯80). Poly(I:C) (50â¯Î¼g) 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.
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Authors
Cheng Zhang, Yun Yu, Jun-feng Yu, Bo-dong Li, Cheng-fan Zhou, Xiao-dong Yang, Xian Wang, Changhao Wu, Tong Shen, Qi-xing Zhu,