RapamycinFungusV1, Main, Exploration, bibRecord, 000335

Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway.

Identifieur interne : 000335 ( Main/Exploration ); précédent : 000334; suivant : 000336

Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway.

Auteurs : Yijuan Shen [République populaire de Chine] ; Nini Zhou [République populaire de Chine] ; Jiahui An [République populaire de Chine] ; Jiansong Zhang [République populaire de Chine] ; Meifen Wang [République populaire de Chine] ; Yufeng Li [République populaire de Chine] ; Ping Jiang [République populaire de Chine]

Source :

Cellular microbiology [ 1462-5822 ] ; 2019.

RBID : pubmed:30977277

Descripteurs français

KwdFr :
- 5-Amino-imidazole-4-carboxamide (analogues et dérivés), 5-Amino-imidazole-4-carboxamide (pharmacologie), AMP-Activated Protein Kinases (génétique), AMP-Activated Protein Kinases (métabolisme), Adénine (analogues et dérivés), Adénine (pharmacologie), Animaux (MeSH), Autophagie (effets des médicaments et des substances chimiques), Autophagie (génétique), Gènes rapporteurs (MeSH), Haemophilus parasuis (croissance et développement), Haemophilus parasuis (métabolisme), Haemophilus parasuis (pathogénicité), Interactions hôte-pathogène (effets des médicaments et des substances chimiques), Interactions hôte-pathogène (génétique), Isoformes de protéines (génétique), Isoformes de protéines (métabolisme), Lignée cellulaire (MeSH), Macrophages alvéolaires (effets des médicaments et des substances chimiques), Macrophages alvéolaires (microbiologie), Macrophages alvéolaires (métabolisme), Oxazines (pharmacologie), Protéines associées aux microtubules (antagonistes et inhibiteurs), Protéines associées aux microtubules (génétique), Protéines associées aux microtubules (métabolisme), Protéines luminescentes (génétique), Protéines luminescentes (métabolisme), Protéines à fluorescence verte (génétique), Protéines à fluorescence verte (métabolisme), Ribonucléotides (pharmacologie), Régulation de l'expression des gènes (MeSH), Sirolimus (pharmacologie), Suidae (MeSH), Transduction du signal (MeSH), Virulence (MeSH).
MESH :
- analogues et dérivés : 5-Amino-imidazole-4-carboxamide, Adénine.
- antagonistes et inhibiteurs : Protéines associées aux microtubules.
- croissance et développement : Haemophilus parasuis.
- effets des médicaments et des substances chimiques : Autophagie, Interactions hôte-pathogène, Macrophages alvéolaires.
- génétique : AMP-Activated Protein Kinases, Autophagie, Interactions hôte-pathogène, Isoformes de protéines, Protéines associées aux microtubules, Protéines luminescentes, Protéines à fluorescence verte.
- microbiologie : Macrophages alvéolaires.
- métabolisme : AMP-Activated Protein Kinases, Haemophilus parasuis, Isoformes de protéines, Macrophages alvéolaires, Protéines associées aux microtubules, Protéines luminescentes, Protéines à fluorescence verte.
- pathogénicité : Haemophilus parasuis.
- pharmacologie : 5-Amino-imidazole-4-carboxamide, Adénine, Oxazines, Ribonucléotides, Sirolimus.
- Animaux, Gènes rapporteurs, Lignée cellulaire, Régulation de l'expression des gènes, Suidae, Transduction du signal, Virulence.

English descriptors

KwdEn :
- AMP-Activated Protein Kinases (genetics), AMP-Activated Protein Kinases (metabolism), Adenine (analogs & derivatives), Adenine (pharmacology), Aminoimidazole Carboxamide (analogs & derivatives), Aminoimidazole Carboxamide (pharmacology), Animals (MeSH), Autophagy (drug effects), Autophagy (genetics), Cell Line (MeSH), Gene Expression Regulation (MeSH), Genes, Reporter (MeSH), Green Fluorescent Proteins (genetics), Green Fluorescent Proteins (metabolism), Haemophilus parasuis (growth & development), Haemophilus parasuis (metabolism), Haemophilus parasuis (pathogenicity), Host-Pathogen Interactions (drug effects), Host-Pathogen Interactions (genetics), Luminescent Proteins (genetics), Luminescent Proteins (metabolism), Macrophages, Alveolar (drug effects), Macrophages, Alveolar (metabolism), Macrophages, Alveolar (microbiology), Microtubule-Associated Proteins (antagonists & inhibitors), Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (metabolism), Oxazines (pharmacology), Protein Isoforms (genetics), Protein Isoforms (metabolism), Ribonucleotides (pharmacology), Signal Transduction (MeSH), Sirolimus (pharmacology), Swine (MeSH), Virulence (MeSH).
MESH :
- chemical , analogs & derivatives : Adenine, Aminoimidazole Carboxamide.
- chemical , antagonists & inhibitors : Microtubule-Associated Proteins.
- chemical , genetics : AMP-Activated Protein Kinases, Green Fluorescent Proteins, Luminescent Proteins, Microtubule-Associated Proteins, Protein Isoforms.
- chemical , metabolism : AMP-Activated Protein Kinases, Green Fluorescent Proteins, Luminescent Proteins, Microtubule-Associated Proteins, Protein Isoforms.
- chemical , pharmacology : Adenine, Aminoimidazole Carboxamide, Oxazines, Ribonucleotides, Sirolimus.
- drug effects : Autophagy, Host-Pathogen Interactions, Macrophages, Alveolar.
- genetics : Autophagy, Host-Pathogen Interactions.
- growth & development : Haemophilus parasuis.
- metabolism : Haemophilus parasuis, Macrophages, Alveolar.
- microbiology : Macrophages, Alveolar.
- pathogenicity : Haemophilus parasuis.
- Animals, Cell Line, Gene Expression Regulation, Genes, Reporter, Signal Transduction, Swine, Virulence.

Abstract

Haemophilus parasuis (H. parasuis) is a common commensal in the upper respiratory tract of pigs, but causes Glässer's disease in stress conditions. To date, many studies focused on the immune evasion and virulence of H. parasuis; very few have focused on the role autophagy played in H. parasuis infection, particularly in porcine alveolar macrophages (PAMs). In this study, a PAM cell line, 3D4/21 cells were used to study the role of autophagy in H. parasuis infection. 3D4/21 cells tandemly expressing GFP, mCherry, and LC3 were infected with H. parasuis serovar 5 (Hps5). Western blot analysis and confocal and transmission electron microscopy showed that H. parasuis infection effectively induces autophagy. Using Hps strains of varying virulence (Hps4, Hps5, and Hps7) and UV-inactivated Hps5, we demonstrated that autophagy is associated with the internalisation of living virulent strains into cells. In 3D4/21 cells pretreated with rapamycin and 3-MA then infected by Hps4, Hps5, and Hps7, we demonstrated that autophagy affects invasion of H. parasuis in cells. AMPK signal results showed that Hps5 infection can upregulate the phosphorylation level of AMPK, which is consistent with the autophagy development. 3D4/21 cells pretreated with AICAR or Compound C then infected by Hps5 revealed that the autophagy induced by Hps5 infection is associated with the AMPK pathway. Our study contributes to the theoretical basis for the study of H. parasuis pathogenesis and development of novel drugs target for prevention Glässer's disease.

DOI: 10.1111/cmi.13031
PubMed: 30977277

Affiliations:

République populaire de Chine

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

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP-Activated Protein Kinases (genetics)</term>
<term>AMP-Activated Protein Kinases (metabolism)</term>
<term>Adenine (analogs & derivatives)</term>
<term>Adenine (pharmacology)</term>
<term>Aminoimidazole Carboxamide (analogs & derivatives)</term>
<term>Aminoimidazole Carboxamide (pharmacology)</term>
<term>Animals (MeSH)</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy (genetics)</term>
<term>Cell Line (MeSH)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Genes, Reporter (MeSH)</term>
<term>Green Fluorescent Proteins (genetics)</term>
<term>Green Fluorescent Proteins (metabolism)</term>
<term>Haemophilus parasuis (growth & development)</term>
<term>Haemophilus parasuis (metabolism)</term>
<term>Haemophilus parasuis (pathogenicity)</term>
<term>Host-Pathogen Interactions (drug effects)</term>
<term>Host-Pathogen Interactions (genetics)</term>
<term>Luminescent Proteins (genetics)</term>
<term>Luminescent Proteins (metabolism)</term>
<term>Macrophages, Alveolar (drug effects)</term>
<term>Macrophages, Alveolar (metabolism)</term>
<term>Macrophages, Alveolar (microbiology)</term>
<term>Microtubule-Associated Proteins (antagonists & inhibitors)</term>
<term>Microtubule-Associated Proteins (genetics)</term>
<term>Microtubule-Associated Proteins (metabolism)</term>
<term>Oxazines (pharmacology)</term>
<term>Protein Isoforms (genetics)</term>
<term>Protein Isoforms (metabolism)</term>
<term>Ribonucleotides (pharmacology)</term>
<term>Signal Transduction (MeSH)</term>
<term>Sirolimus (pharmacology)</term>
<term>Swine (MeSH)</term>
<term>Virulence (MeSH)</term>
</keywords>
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<term>5-Amino-imidazole-4-carboxamide (pharmacologie)</term>
<term>AMP-Activated Protein Kinases (génétique)</term>
<term>AMP-Activated Protein Kinases (métabolisme)</term>
<term>Adénine (analogues et dérivés)</term>
<term>Adénine (pharmacologie)</term>
<term>Animaux (MeSH)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Autophagie (génétique)</term>
<term>Gènes rapporteurs (MeSH)</term>
<term>Haemophilus parasuis (croissance et développement)</term>
<term>Haemophilus parasuis (métabolisme)</term>
<term>Haemophilus parasuis (pathogénicité)</term>
<term>Interactions hôte-pathogène (effets des médicaments et des substances chimiques)</term>
<term>Interactions hôte-pathogène (génétique)</term>
<term>Isoformes de protéines (génétique)</term>
<term>Isoformes de protéines (métabolisme)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Macrophages alvéolaires (effets des médicaments et des substances chimiques)</term>
<term>Macrophages alvéolaires (microbiologie)</term>
<term>Macrophages alvéolaires (métabolisme)</term>
<term>Oxazines (pharmacologie)</term>
<term>Protéines associées aux microtubules (antagonistes et inhibiteurs)</term>
<term>Protéines associées aux microtubules (génétique)</term>
<term>Protéines associées aux microtubules (métabolisme)</term>
<term>Protéines luminescentes (génétique)</term>
<term>Protéines luminescentes (métabolisme)</term>
<term>Protéines à fluorescence verte (génétique)</term>
<term>Protéines à fluorescence verte (métabolisme)</term>
<term>Ribonucléotides (pharmacologie)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Suidae (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
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<term>Green Fluorescent Proteins</term>
<term>Luminescent Proteins</term>
<term>Microtubule-Associated Proteins</term>
<term>Protein Isoforms</term>
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<term>Green Fluorescent Proteins</term>
<term>Luminescent Proteins</term>
<term>Microtubule-Associated Proteins</term>
<term>Protein Isoforms</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenine</term>
<term>Aminoimidazole Carboxamide</term>
<term>Oxazines</term>
<term>Ribonucleotides</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>5-Amino-imidazole-4-carboxamide</term>
<term>Adénine</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines associées aux microtubules</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Host-Pathogen Interactions</term>
<term>Macrophages, Alveolar</term>
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<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
<term>Interactions hôte-pathogène</term>
<term>Macrophages alvéolaires</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term>
<term>Host-Pathogen Interactions</term>
</keywords>
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<term>Interactions hôte-pathogène</term>
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<term>Protéines associées aux microtubules</term>
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<term>Protéines à fluorescence verte</term>
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</keywords>
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</keywords>
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</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>AMP-Activated Protein Kinases</term>
<term>Haemophilus parasuis</term>
<term>Isoformes de protéines</term>
<term>Macrophages alvéolaires</term>
<term>Protéines associées aux microtubules</term>
<term>Protéines luminescentes</term>
<term>Protéines à fluorescence verte</term>
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</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>5-Amino-imidazole-4-carboxamide</term>
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<term>Ribonucléotides</term>
<term>Sirolimus</term>
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<term>Cell Line</term>
<term>Gene Expression Regulation</term>
<term>Genes, Reporter</term>
<term>Signal Transduction</term>
<term>Swine</term>
<term>Virulence</term>
</keywords>
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<term>Gènes rapporteurs</term>
<term>Lignée cellulaire</term>
<term>Régulation de l'expression des gènes</term>
<term>Suidae</term>
<term>Transduction du signal</term>
<term>Virulence</term>
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<front><div type="abstract" xml:lang="en">Haemophilus parasuis (H. parasuis) is a common commensal in the upper respiratory tract of pigs, but causes Glässer's disease in stress conditions. To date, many studies focused on the immune evasion and virulence of H. parasuis; very few have focused on the role autophagy played in H. parasuis infection, particularly in porcine alveolar macrophages (PAMs). In this study, a PAM cell line, 3D4/21 cells were used to study the role of autophagy in H. parasuis infection. 3D4/21 cells tandemly expressing GFP, mCherry, and LC3 were infected with H. parasuis serovar 5 (Hps5). Western blot analysis and confocal and transmission electron microscopy showed that H. parasuis infection effectively induces autophagy. Using Hps strains of varying virulence (Hps4, Hps5, and Hps7) and UV-inactivated Hps5, we demonstrated that autophagy is associated with the internalisation of living virulent strains into cells. In 3D4/21 cells pretreated with rapamycin and 3-MA then infected by Hps4, Hps5, and Hps7, we demonstrated that autophagy affects invasion of H. parasuis in cells. AMPK signal results showed that Hps5 infection can upregulate the phosphorylation level of AMPK, which is consistent with the autophagy development. 3D4/21 cells pretreated with AICAR or Compound C then infected by Hps5 revealed that the autophagy induced by Hps5 infection is associated with the AMPK pathway. Our study contributes to the theoretical basis for the study of H. parasuis pathogenesis and development of novel drugs target for prevention Glässer's disease.</div>
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<DateCompleted><Year>2020</Year>
<Month>08</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>08</Month>
<Day>28</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1462-5822</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>21</Volume>
<Issue>8</Issue>
<PubDate><Year>2019</Year>
<Month>08</Month>
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<Title>Cellular microbiology</Title>
<ISOAbbreviation>Cell Microbiol</ISOAbbreviation>
</Journal>
<ArticleTitle>Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway.</ArticleTitle>
<Pagination><MedlinePgn>e13031</MedlinePgn>
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<Abstract><AbstractText>Haemophilus parasuis (H. parasuis) is a common commensal in the upper respiratory tract of pigs, but causes Glässer's disease in stress conditions. To date, many studies focused on the immune evasion and virulence of H. parasuis; very few have focused on the role autophagy played in H. parasuis infection, particularly in porcine alveolar macrophages (PAMs). In this study, a PAM cell line, 3D4/21 cells were used to study the role of autophagy in H. parasuis infection. 3D4/21 cells tandemly expressing GFP, mCherry, and LC3 were infected with H. parasuis serovar 5 (Hps5). Western blot analysis and confocal and transmission electron microscopy showed that H. parasuis infection effectively induces autophagy. Using Hps strains of varying virulence (Hps4, Hps5, and Hps7) and UV-inactivated Hps5, we demonstrated that autophagy is associated with the internalisation of living virulent strains into cells. In 3D4/21 cells pretreated with rapamycin and 3-MA then infected by Hps4, Hps5, and Hps7, we demonstrated that autophagy affects invasion of H. parasuis in cells. AMPK signal results showed that Hps5 infection can upregulate the phosphorylation level of AMPK, which is consistent with the autophagy development. 3D4/21 cells pretreated with AICAR or Compound C then infected by Hps5 revealed that the autophagy induced by Hps5 infection is associated with the AMPK pathway. Our study contributes to the theoretical basis for the study of H. parasuis pathogenesis and development of novel drugs target for prevention Glässer's disease.</AbstractText>
<CopyrightInformation>© 2019 John Wiley & Sons Ltd.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shen</LastName>
<ForeName>Yijuan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Bacteriology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.</Affiliation>
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<Initials>N</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Bacteriology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.</Affiliation>
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<ForeName>Jiahui</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Bacteriology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.</Affiliation>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Jiansong</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Bacteriology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.</Affiliation>
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<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Meifen</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Bacteriology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.</Affiliation>
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<ForeName>Ping</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Key Laboratory of Bacteriology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.</Affiliation>
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<Language>eng</Language>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>04</Month>
<Day>26</Day>
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</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Cell Microbiol</MedlineTA>
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<ISSNLinking>1462-5814</ISSNLinking>
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<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
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Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway.

Haemophilus parasuis infection in 3D4/21 cells induces autophagy through the AMPK pathway.

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