Differential regulation of TLR signaling on the induction of antiviral interferons in human intestinal epithelial cells infected with Enterovirus 71

Chunyang Wang, Lianfu Ji, Xinhui Yuan, Yu Jin, Carol J. Cardona, Zheng Xing

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Enterovirus 71 (EV71) causes hand-foot-and-mouth disease, which can lead to fatal neurological complications in young children and infants. Few gastrointestinal symptoms are observed clinically, suggesting the presence of a unique immunity to EV71 in the gut. We reported a robust induction of interferons (IFNs) in human intestinal epithelial cells (HT-29), which was suppressed in other types such as RD and HeLa cells. The underlying mechanism for the apparent difference remains obscure. In this study we report that in EV71-infected HT-29 cells, TLR/TRIF signaling was essential to IFN induction; viral replication increased and the induction of IFN-α, -β, -ω, -κ, and -ε decreased markedly in TRIF-silenced HT-29 cells. Importantly, TRIF was degraded by viral 3Cpro in RD cells, but resisted cleavage, and IRF3 was activated and translocated into the nucleus in HT-29 cells. Taken together, our data suggest that IFNs were induced differentially in human HT-29 cells through an intact TLR/TRIF signaling, which differs from other cell types and may be implicated in viral pathogenesis in EV71 infection.

Original languageEnglish (US)
Article numbere0152177
JournalPloS one
Volume11
Issue number3
DOIs
StatePublished - Mar 2016

Bibliographical note

Funding Information:
This work was supported by a funding from National Natural Science Foundation of China (No. 81571993) and a Mega Infectious Diseases Program from the Ministry of Science of Technology of China (Grant No. 2014ZX10004001-002) to Z.X. and a Natural Science Foundation of Jiangsu Province (BK20141078) to Y.J. We thank Ms. Sandy Shanks for her dedicated and excellent work in editing the manuscript.

Publisher Copyright:
© 2016 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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