ROS induced by spring viraemia of carp virus activate the inflammatory response via the MAPK/AP-1 and PI3K signaling pathways.

Autor: Sun J; Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China., Wang J; Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China., Li L; Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China; Hubei Engineering Research Center for Aquatic Animal Diseases Control and Prevention, Wuhan, 430070, People's Republic of China., Wu Z; Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China; Hubei Engineering Research Center for Aquatic Animal Diseases Control and Prevention, Wuhan, 430070, People's Republic of China., Chen X; Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China; Hubei Engineering Research Center for Aquatic Animal Diseases Control and Prevention, Wuhan, 430070, People's Republic of China., Yuan J; Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China; Hubei Engineering Research Center for Aquatic Animal Diseases Control and Prevention, Wuhan, 430070, People's Republic of China; Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Wuhan, 430070, People's Republic of China. Electronic address: jfyuan@mail.hzau.edu.cn.
Jazyk: angličtina
Zdroj: Fish & shellfish immunology [Fish Shellfish Immunol] 2020 Jun; Vol. 101, pp. 216-224. Date of Electronic Publication: 2020 Mar 26.
DOI: 10.1016/j.fsi.2020.03.056
Abstrakt: Spring viraemia of carp virus (SVCV) can cause a high mortality in common carp (Cyprinus carpio), and its main pathological processes include the inflammatory response. However, the detailed mechanism is still unclear. Reactive oxygen species (ROS) have been shown to play critical roles in the immune response, including inflammation, in different models. Our previous studies have demonstrated that SVCV infection results in the accumulation of ROS, including H 2 O 2 , in epithelioma papulosum cyprini (EPC) cells. In this study, we aimed to explore the relationship between H 2 O 2 accumulation and inflammation during SVCV infection. After EPC cells were infected with SVCV, the expression levels of the inflammatory factors tumor necrosis factor (TNF)-α, cyclooxygenase (COX)-2, and interleukin (IL)-8 were up-regulated, while the expression of the anti-inflammatory factor interleukin (IL)-10 was down-regulated, compared with that in mock-infected EPC cells. The antioxidant N-acetyl-l-cysteine (NAC) could dampen the increased TNF-ɑ and COX-2 expression induced by SVCV and H 2 O 2 , suggesting a relationship between ROS accumulation and inflammation during SVCV infection. Dual luciferase reporter assays demonstrated that SVCV could not activate the NF-κB pathway. In addition, inhibition of NF-κB by pyrrolidine dithiocarbamate (PDTC) treatment had no effect on the expression of inflammatory factors. Furthermore, inhibition of the ERK, JNK, and p38MAPK signaling pathways by U0126, SP600125, and SB203580, respectively, reduced the expression of TNF-ɑ, COX-2, and IL-8, indicating that these three signaling pathways were all involved in the inflammatory response after SVCV infection. In addition, the PI3K signaling pathway was involved in the expression of the chemokine IL-8 in the SVCV-induced inflammatory response. We also showed that inhibition of the MAPK or PI3K signaling pathway facilitated the expression of SVCV-G as well as increased the SVCV viral titer. Altogether these results reveal the mechanism of the SVCV-mediated inflammatory response. Thus, targeting these signaling pathways may provide novel treatment strategies for SVCV-mediated diseases.
Competing Interests: Declaration of competing interest The authors declare no financial or commercial conflicts of interest.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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