Abstract
Porcine circovirus type 2 (PCV2) causes porcine circovirus-associated diseases and usually evokes a subclinical infection, without any obvious symptoms, in pigs. It remains unclear how PCV2 leads to a subclinical infection. In this study, we found that peripheral blood mononuclear cells (PBMCs) from PCV2-challenged piglets with no significant clinical symptoms exhibited increased expression of suppressor of cytokine signaling (SOCS) 3, but no significant changes in the expression of the proinflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α; this differed from piglets that displayed significant clinical symptoms. IL-6- and TNF-α-mediated signalings were inhibited in PBMCs from subclinical piglets. Elevated SOCS3 levels inhibited IL-6- and TNF-α-mediated NF-kappa-B inhibitor alpha degradation in PBMCs and PK-15 cells. SOCS3 production was also increased in PCV2-infected PK-15 porcine kidney cells, and IL-6 and TNF-α production that was induced by PCV2 in PK-15 cells was significantly increased when SOCS3 was silenced by a small interfering RNA. SOCS3 interacted with signal transducer and activator of transcription 3 and TNF-associated receptor-associated factor 2, suggesting mechanisms by which SOCS3 inhibits IL-6 and TNF-α signaling. We conclude that SOCS3 plays an important role in PCV2 subclinical infection by suppressing inflammatory responses in primary immune cells.
Highlights
Infected piglets at 0–4 weeks post-challenge were measured by real-time RT-PCR
Endogenous SOCS3 (B), IL-6 (C), and tumor necrosis factor (TNF)-α(D) mRNA levels were measured in Peripheral blood mononuclear cells (PBMCs) from subclinical Porcine circovirus type 2 (PCV2)-infected piglets at 0, 2, and 4 weeks post-challenge by real-time RT-PCR (n = 11). (E) Viral loads of PBMCs separated from post-weaning multisystemic wasting syndrome (PMWS) piglets at 0–4 weeks
We found that the expression levels of SOCS3, IL-6, and TNF-αin PBMCs differed between piglets with PMWS and subclinical PCV2-infected piglets, and that SOCS3 plays an important role in regulating proinflammatory cytokines in subclinical PCV2 infections
Summary
Infected piglets at 0–4 weeks post-challenge were measured by real-time RT-PCR. Endogenous SOCS3 (B), IL-6 (C), and TNF-α(D) mRNA levels were measured in PBMCs from subclinical PCV2-infected piglets at 0, 2, and 4 weeks post-challenge by real-time RT-PCR (n = 11). Endogenous SOCS3 (F), IL-6 (G), and TNF-α(H) mRNA levels were measured in PBMCs from PMWS piglets (n = 5). TNF-αand IL-6 induce SOCS3 expression, and SOCS3 plays an important role in the negative feedback of some proinflammatory signal transducers such as TNF-αand IL-628. We found that the expression levels of SOCS3, IL-6, and TNF-αin PBMCs differed between piglets with PMWS and subclinical PCV2-infected piglets, and that SOCS3 plays an important role in regulating proinflammatory cytokines in subclinical PCV2 infections
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have