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Rapamycin-induced autophagy restricts porcine epidemic diarrhea virus infectivity in porcine intestinal epithelial cells.

Authors
  • Ko, Seongyeol1
  • Gu, Min Jeong1
  • Kim, Cheol Gyun1
  • Kye, Yoon Chul1
  • Lim, Younggap1
  • Lee, Ji Eun1
  • Park, Byung-Chul2
  • Chu, Hyuk3
  • Han, Seung Hyun4
  • Yun, Cheol-Heui5
  • 1 Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea. , (North Korea)
  • 2 Institute of Green Bio Science Technology, Seoul National University, Pyeongchang 23254, Republic of Korea. , (North Korea)
  • 3 Division of Zoonoses, Center for Immunology and Pathology, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong 28159, Republic of Korea. , (North Korea)
  • 4 Department of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, School of Dentistry, Seoul National University, Seoul 08826, Republic of Korea. , (North Korea)
  • 5 Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea; Institute of Green Bio Science Technology, Seoul National University, Pyeongchang 23254, Republic of Korea. Electronic address: [email protected] , (North Korea)
Type
Published Article
Journal
Antiviral research
Publication Date
Oct 01, 2017
Volume
146
Pages
86–95
Identifiers
DOI: 10.1016/j.antiviral.2017.08.010
PMID: 28842266
Source
Medline
Keywords
License
Unknown

Abstract

Porcine epidemic diarrhea virus (PEDV) invades porcine intestinal epithelial cells (IECs) and causes diarrhea and dehydration in pigs. In the present study, we showed a suppression of PEDV infection in porcine jejunum intestinal epithelial cells (IPEC-J2) by an increase in autophagy. Autophagy was activated by rapamycin at a dose that does not affect cell viability and tight junction permeability. The induction of autophagy was examined by LC3I/LC3II conversion. To confirm the autophagic-flux (entire autophagy pathway), autophagolysosomes were examined by an immunofluorescence assay. Pre-treatment with rapamycin significantly restricted not only a 1 h infection but also a longer infection (24 h) with PEDV, while this effect disappeared when autophagy was blocked. Co-localization of PEDV and autophagosomes suggests that PEDV could be a target of autophagy. Moreover, alleviation of PEDV-induced cell death in IPEC-J2 cells pretreated with rapamycin demonstrates a protective effect of rapamycin against PEDV-induced epithelial cell death. Collectively, the present study suggests an early prevention against PEDV infection in IPEC-J2 cells via autophagy that might be an effective strategy for the restriction of PEDV, and opens up the possibility of the use of rapamycin in vivo as an effective prophylactic and prevention treatment.

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