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Hypothalamus-pituitary-adrenal axis involves in anti-viral ability through regulation of immune response in piglets infected by highly pathogenic porcine reproductive and respiratory syndrome virus

Author:
Tong, Jie, Yu, Ying, Zheng, Linlin, Zhang, Chong, Tu, Yabin, Liu, Yonggang, Wu, Jianan, Li, Hai, Wang, Shujie, Jiang, Chenggang, Zhou, En-Min, Wang, Gang, Cai, Xuehui
Source:
BMC veterinary research 2018 v.14 no.1 pp. 92
ISSN:
1746-6148
Subject:
Porcine reproductive and respiratory syndrome virus, blood, body weight, burden of disease, cytokines, dexamethasone, disease severity, etiology, immune response, immune system, industry, lungs, mortality, piglets, veterinary medicine, China
Abstract:
BACKGROUND: The highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) has been responsible for several viral attacks in the Asian porcine industry, since the first outbreak in China in 2006. During the early stages of the HP-PRRSV infection, high levels of proinflammatory cytokines are noted in the host peripheral blood, which are accompanied by severe lesions in the lungs and immune system organs; these are considered as the greatest contributors to the overall disease burden. We hypothesized that the anti-PRRSV response in piglets might be mediated by the hypothalamus-pituitary-adrenal (HPA) axis, which led to a decrease in the psycho-neuroendocrinological manifestation of HP-PRRSV etiology via immune response regulation. RESULTS: We investigated the regulation of the HPA axis in HP-PRRSV-infected piglets that were treated with 1 mg/kg body weight (b. w.)/day mifepristone (RU486) or 2 mg/kg b.w./day dexamethasone (DEX). Both RU486 and DEX enhanced the disease status of the piglets infected by the HP-PRRSV HuN4 strain, resulting in high mortality and more severe pathological changes in the lungs. CONCLUSIONS: HP-PRRSV infection activates the HPA axis, and artificial regulation of the immune-endocrine system enhances disease severity in HP-PRRSV-infected piglets. Thus, DEX and RU486 should be avoided in the clinical treatment of HP-PRRS.
Agid:
5911326