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Transmissible gastroenteritis virus does not suppress IFN-? induction but is sensitive to IFN in IPEC-J2 cells.

ABSTRACT: Coronaviruses tend to efficiently evade innate immune sensing. Alpha-coronaviruses interfere with the type I interferon (IFN) response in various ways, ensuring the limited activation of IFN responses. Transmissible gastroenteritis virus (TGEV), an Alphacoronavirus genera virus, is an important pathogen that mainly infects piglet, but little is known about the activation of the host immune response. We show that TGEV induces a delayed activation of the IFN response in intestinal epithelial cells. Briefly, IFN-? expression induced by TGEV infection is delayed with respect to that induced by poly(I:C) transfection. In addition, some of the IFN-stimulated genes (ISGs) were up-regulated in the early infection stage without obvious expression of IFN-?. Moreover, we show that activation of IFN responses induced by poly(I:C) could inhibit viral replication in the early infection stage, but failed in the late infection stage in IPEC-J2 cells. Finally, the activation of IFN responses induced by TGEV infection cannot inhibit viral replication. Taken together, this study provides a preliminary analysis of an interaction between TGEV and IFN-? responses of intestinal epithelial cells.

SUBMITTER: Zhu L

PROVIDER: S-EPMC7117263 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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Transmissible gastroenteritis virus does not suppress IFN-β induction but is sensitive to IFN in IPEC-J2 cells.

Zhu Liqi L Yang Xing X Mou Chunxiao C Yang Qian Q

Veterinary microbiology 20161221

Coronaviruses tend to efficiently evade innate immune sensing. Alpha-coronaviruses interfere with the type I interferon (IFN) response in various ways, ensuring the limited activation of IFN responses. Transmissible gastroenteritis virus (TGEV), an Alphacoronavirus genera virus, is an important pathogen that mainly infects piglet, but little is known about the activation of the host immune response. We show that TGEV induces a delayed activation of the IFN response in intestinal epithelial cells ...[more]

PMID: 28110779

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Project description:Transmissible gastroenteritis virus (TGEV) infection can cause transmissible gastroenteritis (TGE), especially in suckling piglets, resulting in a significant economic loss for the global pig industry. The pathogenesis of TGEV infection is closely related to intestinal inflammation. All-trans retinoic acid (ATRA) has anti-inflammatory activity and immunomodulatory properties, but it is unclear whether ATRA can attenuate the inflammatory response induced by TGEV. This study aimed to investigate the protective effect of ATRA on TGEV-induced inflammatory injury in intestinal porcine epithelial cells (IPEC-J2) and to explore the underlying molecular mechanism. The results showed that TGEV infection triggered inflammatory response and damaged epithelial barrier integrity in IPEC-J2 cells. However, ATRA attenuated TGEV-induced inflammatory response by inhibiting the release of pro-inflammatory cytokines, including IL-1β, IL-6, IL-8 and TNF-α. ATRA also significantly reversed the reduction of ZO-1 and Occludin protein levels induced by TGEV infection and maintained epithelial barrier integrity. Moreover, ATRA treatment significantly prevented the upregulation of IкBα and NF-κB p65 phosphorylation levels and the nuclear translocation of NF-кB p65 induced by TGEV. On the other hand, treatment of TGEV-infected IPEC-J2 cells with the NF-κB inhibitors (BAY11-7082) significantly decreased the levels of inflammatory cytokines. Furthermore, ATRA treatment significantly downregulated the mRNA abundance and protein levels of TLR3, TLR7, RIG-I and MDA5, and downregulated their downstream signaling molecules TRIF, TRAF6 and MAVS mRNA expressions in TGEV-infected IPEC-J2 cells. However, the knockdown of RIG-I and MDA5 but not TLR3 and TLR7 significantly reduced the NF-κB p65 phosphorylation level and inflammatory cytokines levels in TGEV-infected IPEC-J2 cells. Our results indicated that ATRA attenuated TGEV-induced IPEC-J2 cells damage via suppressing inflammatory response, the mechanism of which is associated with the inhibition of TGEV-mediated activation of the RLRs/NF-κB signaling pathway.

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Transmissible gastroenteritis virus does not suppress IFN-? induction but is sensitive to IFN in IPEC-J2 cells.

Publications

Transmissible gastroenteritis virus does not suppress IFN-β induction but is sensitive to IFN in IPEC-J2 cells.

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