RapamycinFungusV1, Main, Exploration, bibRecord, 000760

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

Identifieur interne : 000760 ( Main/Exploration ); précédent : 000759; suivant : 000761

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

Auteurs : Seongyeol Ko [Corée du Sud] ; Min Jeong Gu [Corée du Sud] ; Cheol Gyun Kim [Corée du Sud] ; Yoon Chul Kye [Corée du Sud] ; Younggap Lim [Corée du Sud] ; Ji Eun Lee [Corée du Sud] ; Byung-Chul Park [Corée du Sud] ; Hyuk Chu [Corée du Sud] ; Seung Hyun Han [Corée du Sud] ; Cheol-Heui Yun [Corée du Sud]

Source :

Antiviral research [ 1872-9096 ] ; 2017.

RBID : pubmed:28842266

Descripteurs français

KwdFr :
- Animaux (MeSH), Antiviraux (pharmacologie), Autophagie (MeSH), Cellules Vero (MeSH), Cellules épithéliales (effets des médicaments et des substances chimiques), Cellules épithéliales (virologie), Infections à coronavirus (traitement médicamenteux), Interactions hôte-pathogène (MeSH), Intestins (cytologie), Intestins (effets des médicaments et des substances chimiques), Intestins (virologie), Lignée cellulaire (MeSH), Mort cellulaire (effets des médicaments et des substances chimiques), Sirolimus (pharmacologie), Suidae (MeSH), Virus de la diarrhée porcine épidémique (effets des médicaments et des substances chimiques), Virus de la diarrhée porcine épidémique (physiologie).
MESH :
- cytologie : Intestins.
- effets des médicaments et des substances chimiques : Cellules épithéliales, Intestins, Mort cellulaire, Virus de la diarrhée porcine épidémique.
- pharmacologie : Antiviraux, Sirolimus.
- physiologie : Virus de la diarrhée porcine épidémique.
- traitement médicamenteux : Infections à coronavirus.
- virologie : Cellules épithéliales, Intestins.
- Animaux, Autophagie, Cellules Vero, Interactions hôte-pathogène, Lignée cellulaire, Suidae.

English descriptors

KwdEn :
- Animals (MeSH), Antiviral Agents (pharmacology), Autophagy (MeSH), Cell Death (drug effects), Cell Line (MeSH), Chlorocebus aethiops (MeSH), Coronavirus Infections (drug therapy), Epithelial Cells (drug effects), Epithelial Cells (virology), Host-Pathogen Interactions (MeSH), Intestines (cytology), Intestines (drug effects), Intestines (virology), Porcine epidemic diarrhea virus (drug effects), Porcine epidemic diarrhea virus (physiology), Sirolimus (pharmacology), Swine (MeSH), Vero Cells (MeSH).
MESH :
- chemical , pharmacology : Antiviral Agents, Sirolimus.
- cytology : Intestines.
- drug effects : Cell Death, Epithelial Cells, Intestines, Porcine epidemic diarrhea virus.
- drug therapy : Coronavirus Infections.
- physiology : Porcine epidemic diarrhea virus.
- virology : Epithelial Cells, Intestines.
- Animals, Autophagy, Cell Line, Chlorocebus aethiops, Host-Pathogen Interactions, Swine, Vero Cells.

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.

DOI: 10.1016/j.antiviral.2017.08.010
PubMed: 28842266
PubMed Central: PMC7113733

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000744
to stream Main, to step Curation: 000744

Le document en format XML

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<term>Antiviral Agents (pharmacology)</term>
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<front><div type="abstract" xml:lang="en">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.</div>
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<DateCompleted><Year>2018</Year>
<Month>07</Month>
<Day>17</Day>
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<DateRevised><Year>2020</Year>
<Month>04</Month>
<Day>07</Day>
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<JournalIssue CitedMedium="Internet"><Volume>146</Volume>
<PubDate><Year>2017</Year>
<Month>Oct</Month>
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<Title>Antiviral research</Title>
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<ArticleTitle>Rapamycin-induced autophagy restricts porcine epidemic diarrhea virus infectivity in porcine intestinal epithelial cells.</ArticleTitle>
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<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>Copyright © 2017 Elsevier B.V. All rights reserved.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ko</LastName>
<ForeName>Seongyeol</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Agricultural Biotechnology and Research Institute for Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea.</Affiliation>
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<Author ValidYN="Y"><LastName>Gu</LastName>
<ForeName>Min Jeong</ForeName>
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</AffiliationInfo>
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</AffiliationInfo>
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<ForeName>Seung Hyun</ForeName>
<Initials>SH</Initials>
<AffiliationInfo><Affiliation>Department of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, School of Dentistry, Seoul National University, Seoul 08826, Republic of Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yun</LastName>
<ForeName>Cheol-Heui</ForeName>
<Initials>CH</Initials>
<AffiliationInfo><Affiliation>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: cyun@snu.ac.kr.</Affiliation>
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<Language>eng</Language>
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<Month>08</Month>
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	Serveur d'exploration sur la rapamycine et les champignons
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Rapamycin-induced autophagy restricts porcine epidemic diarrhea virus infectivity in porcine intestinal epithelial cells.

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

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