RapamycinFungusV1, Main, Exploration, bibRecord, 000A39

Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.

Identifieur interne : 000A39 ( Main/Exploration ); précédent : 000A38; suivant : 000A40

Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.

Auteurs : Yongjian Wu [République populaire de Chine] ; Dandan Li [République populaire de Chine] ; Yi Wang [République populaire de Chine] ; Kang Chen [République populaire de Chine] ; Kun Yang [République populaire de Chine] ; Xi Huang [République populaire de Chine] ; Yuanqing Zhang [République populaire de Chine] ; Minhao Wu [République populaire de Chine]

Source :

International immunopharmacology [ 1878-1705 ] ; 2016.

RBID : pubmed:27295610

Descripteurs français

KwdFr :
- Animaux (MeSH), Autophagie (génétique), Bécline-1 (génétique), Bécline-1 (métabolisme), Cellules RAW 264.7 (MeSH), Espèces réactives de l'oxygène (métabolisme), Humains (MeSH), Immunité innée (génétique), Infections à Pseudomonas (immunologie), Macrophages (microbiologie), Macrophages (physiologie), Monoxyde d'azote (métabolisme), Petit ARN interférent (génétique), Protéine-7 associée à l'autophagie (génétique), Protéine-7 associée à l'autophagie (métabolisme), Pseudomonas aeruginosa (immunologie), Souris (MeSH), Échappement immunitaire (génétique).
MESH :
- génétique : Autophagie, Bécline-1, Immunité innée, Petit ARN interférent, Protéine-7 associée à l'autophagie, Échappement immunitaire.
- immunologie : Infections à Pseudomonas, Pseudomonas aeruginosa.
- microbiologie : Macrophages.
- métabolisme : Bécline-1, Espèces réactives de l'oxygène, Monoxyde d'azote, Protéine-7 associée à l'autophagie.
- physiologie : Macrophages.
- Animaux, Cellules RAW 264.7, Humains, Souris.

English descriptors

KwdEn :
- Animals (MeSH), Autophagy (genetics), Autophagy-Related Protein 7 (genetics), Autophagy-Related Protein 7 (metabolism), Beclin-1 (genetics), Beclin-1 (metabolism), Humans (MeSH), Immune Evasion (genetics), Immunity, Innate (genetics), Macrophages (microbiology), Macrophages (physiology), Mice (MeSH), Nitric Oxide (metabolism), Pseudomonas Infections (immunology), Pseudomonas aeruginosa (immunology), RAW 264.7 Cells (MeSH), RNA, Small Interfering (genetics), Reactive Oxygen Species (metabolism).
MESH :
- chemical , genetics : Autophagy-Related Protein 7, Beclin-1, RNA, Small Interfering.
- genetics : Autophagy, Immune Evasion, Immunity, Innate.
- immunology : Pseudomonas Infections, Pseudomonas aeruginosa.
- chemical , metabolism : Autophagy-Related Protein 7, Beclin-1, Nitric Oxide, Reactive Oxygen Species.
- microbiology : Macrophages.
- physiology : Macrophages.
- Animals, Humans, Mice, RAW 264.7 Cells.

Abstract

OBJECTIVES

To explore the role of autophagy on macrophage-mediated phagocytosis and intracellular killing of Pseudomonas aeruginosa (PA), a common extracellular bacterium which often causes various opportunistic infections.

METHODS

Macrophages were infected with PA or stimulated with zymosan bioparticles. Autophagy was tested by fluorescent microscopy and Western blot for LC3. Phagocytosis and killing efficiency were assessed by plate count assay, flow cytometry or immunofluorescent staining. Phagocytic receptor expression, ROS generation and NO production were examined by PCR, flow cytometry and Griess reaction, respectively.

RESULTS

PA infection induced autophagy activation in both mouse and human macrophages. Induction of autophagy by rapamycin or starvation significantly inhibited PA internalization by downregulating phagocytosis receptor expression, and suppressed intracellular killing of PA via reducing ROS and NO production in macrophages. While knockdown of autophagy molecules ATG7 or Beclin1 enhanced macrophage-mediated phagocytosis and intracellular killing of PA. Additionally, confocal microscopy data showed that induction of autophagy reduced the number of phagosomes and phagolysosomes in macrophages after stimulation with zymosan bioparticles.

CONCLUSIONS

Our study suggested that PA promotes autophagy to suppress macrophage-mediated bacterial phagocytosis and intracellular killing. These insights demonstrated a novel immune evasion mechanism employed by PA, which may provide potential therapeutic strategies of PA infectious diseases.

DOI: 10.1016/j.intimp.2016.04.044
PubMed: 27295610

Affiliations:

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

to stream Main, to step Corpus: 000A32
to stream Main, to step Curation: 000A32

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.</title>
<author><name sortKey="Wu, Yongjian" sort="Wu, Yongjian" uniqKey="Wu Y" first="Yongjian" last="Wu">Yongjian Wu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Li, Dandan" sort="Li, Dandan" uniqKey="Li D" first="Dandan" last="Li">Dandan Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 243000, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Clinical Laboratory, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 243000</wicri:regionArea>
<wicri:noRegion>Nanjing 243000</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Chen, Kang" sort="Chen, Kang" uniqKey="Chen K" first="Kang" last="Chen">Kang Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China; Division of Clinical Laboratory, Zhongshan Hospital of Sun Yat-sen University, Zhongshan 528403, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China; Division of Clinical Laboratory, Zhongshan Hospital of Sun Yat-sen University, Zhongshan 528403</wicri:regionArea>
<wicri:noRegion>Zhongshan 528403</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yang, Kun" sort="Yang, Kun" uniqKey="Yang K" first="Kun" last="Yang">Kun Yang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Huang, Xi" sort="Huang, Xi" uniqKey="Huang X" first="Xi" last="Huang">Xi Huang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Zhang, Yuanqing" sort="Zhang, Yuanqing" uniqKey="Zhang Y" first="Yuanqing" last="Zhang">Yuanqing Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: zyqsinap@gmail.com.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wu, Minhao" sort="Wu, Minhao" uniqKey="Wu M" first="Minhao" last="Wu">Minhao Wu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China. Electronic address: wuminhao@mail.sysu.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2016">2016</date>
<idno type="RBID">pubmed:27295610</idno>
<idno type="pmid">27295610</idno>
<idno type="doi">10.1016/j.intimp.2016.04.044</idno>
<idno type="wicri:Area/Main/Corpus">000A32</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000A32</idno>
<idno type="wicri:Area/Main/Curation">000A32</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000A32</idno>
<idno type="wicri:Area/Main/Exploration">000A32</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.</title>
<author><name sortKey="Wu, Yongjian" sort="Wu, Yongjian" uniqKey="Wu Y" first="Yongjian" last="Wu">Yongjian Wu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Li, Dandan" sort="Li, Dandan" uniqKey="Li D" first="Dandan" last="Li">Dandan Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Laboratory, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 243000, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Clinical Laboratory, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 243000</wicri:regionArea>
<wicri:noRegion>Nanjing 243000</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Chen, Kang" sort="Chen, Kang" uniqKey="Chen K" first="Kang" last="Chen">Kang Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China; Division of Clinical Laboratory, Zhongshan Hospital of Sun Yat-sen University, Zhongshan 528403, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China; Division of Clinical Laboratory, Zhongshan Hospital of Sun Yat-sen University, Zhongshan 528403</wicri:regionArea>
<wicri:noRegion>Zhongshan 528403</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yang, Kun" sort="Yang, Kun" uniqKey="Yang K" first="Kun" last="Yang">Kun Yang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Huang, Xi" sort="Huang, Xi" uniqKey="Huang X" first="Xi" last="Huang">Xi Huang</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Zhang, Yuanqing" sort="Zhang, Yuanqing" uniqKey="Zhang Y" first="Yuanqing" last="Zhang">Yuanqing Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: zyqsinap@gmail.com.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wu, Minhao" sort="Wu, Minhao" uniqKey="Wu M" first="Minhao" last="Wu">Minhao Wu</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China. Electronic address: wuminhao@mail.sysu.edu.cn.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080</wicri:regionArea>
<placeName><settlement type="city">Jiangmen</settlement>
<region type="province">Guangdong</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">International immunopharmacology</title>
<idno type="eISSN">1878-1705</idno>
<imprint><date when="2016" type="published">2016</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Autophagy (genetics)</term>
<term>Autophagy-Related Protein 7 (genetics)</term>
<term>Autophagy-Related Protein 7 (metabolism)</term>
<term>Beclin-1 (genetics)</term>
<term>Beclin-1 (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Immune Evasion (genetics)</term>
<term>Immunity, Innate (genetics)</term>
<term>Macrophages (microbiology)</term>
<term>Macrophages (physiology)</term>
<term>Mice (MeSH)</term>
<term>Nitric Oxide (metabolism)</term>
<term>Pseudomonas Infections (immunology)</term>
<term>Pseudomonas aeruginosa (immunology)</term>
<term>RAW 264.7 Cells (MeSH)</term>
<term>RNA, Small Interfering (genetics)</term>
<term>Reactive Oxygen Species (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Autophagie (génétique)</term>
<term>Bécline-1 (génétique)</term>
<term>Bécline-1 (métabolisme)</term>
<term>Cellules RAW 264.7 (MeSH)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Immunité innée (génétique)</term>
<term>Infections à Pseudomonas (immunologie)</term>
<term>Macrophages (microbiologie)</term>
<term>Macrophages (physiologie)</term>
<term>Monoxyde d'azote (métabolisme)</term>
<term>Petit ARN interférent (génétique)</term>
<term>Protéine-7 associée à l'autophagie (génétique)</term>
<term>Protéine-7 associée à l'autophagie (métabolisme)</term>
<term>Pseudomonas aeruginosa (immunologie)</term>
<term>Souris (MeSH)</term>
<term>Échappement immunitaire (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Autophagy-Related Protein 7</term>
<term>Beclin-1</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term>
<term>Immune Evasion</term>
<term>Immunity, Innate</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Autophagie</term>
<term>Bécline-1</term>
<term>Immunité innée</term>
<term>Petit ARN interférent</term>
<term>Protéine-7 associée à l'autophagie</term>
<term>Échappement immunitaire</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections à Pseudomonas</term>
<term>Pseudomonas aeruginosa</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Pseudomonas Infections</term>
<term>Pseudomonas aeruginosa</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autophagy-Related Protein 7</term>
<term>Beclin-1</term>
<term>Nitric Oxide</term>
<term>Reactive Oxygen Species</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term>
<term>Espèces réactives de l'oxygène</term>
<term>Monoxyde d'azote</term>
<term>Protéine-7 associée à l'autophagie</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Macrophages</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Humans</term>
<term>Mice</term>
<term>RAW 264.7 Cells</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules RAW 264.7</term>
<term>Humains</term>
<term>Souris</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b>
</p>
<p>To explore the role of autophagy on macrophage-mediated phagocytosis and intracellular killing of Pseudomonas aeruginosa (PA), a common extracellular bacterium which often causes various opportunistic infections.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>Macrophages were infected with PA or stimulated with zymosan bioparticles. Autophagy was tested by fluorescent microscopy and Western blot for LC3. Phagocytosis and killing efficiency were assessed by plate count assay, flow cytometry or immunofluorescent staining. Phagocytic receptor expression, ROS generation and NO production were examined by PCR, flow cytometry and Griess reaction, respectively.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>PA infection induced autophagy activation in both mouse and human macrophages. Induction of autophagy by rapamycin or starvation significantly inhibited PA internalization by downregulating phagocytosis receptor expression, and suppressed intracellular killing of PA via reducing ROS and NO production in macrophages. While knockdown of autophagy molecules ATG7 or Beclin1 enhanced macrophage-mediated phagocytosis and intracellular killing of PA. Additionally, confocal microscopy data showed that induction of autophagy reduced the number of phagosomes and phagolysosomes in macrophages after stimulation with zymosan bioparticles.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>Our study suggested that PA promotes autophagy to suppress macrophage-mediated bacterial phagocytosis and intracellular killing. These insights demonstrated a novel immune evasion mechanism employed by PA, which may provide potential therapeutic strategies of PA infectious diseases.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27295610</PMID>
<DateCompleted><Year>2017</Year>
<Month>04</Month>
<Day>06</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>04</Month>
<Day>06</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-1705</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>38</Volume>
<PubDate><Year>2016</Year>
<Month>Sep</Month>
</PubDate>
</JournalIssue>
<Title>International immunopharmacology</Title>
<ISOAbbreviation>Int Immunopharmacol</ISOAbbreviation>
</Journal>
<ArticleTitle>Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.</ArticleTitle>
<Pagination><MedlinePgn>214-22</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.intimp.2016.04.044</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S1567-5769(16)30187-4</ELocationID>
<Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">To explore the role of autophagy on macrophage-mediated phagocytosis and intracellular killing of Pseudomonas aeruginosa (PA), a common extracellular bacterium which often causes various opportunistic infections.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Macrophages were infected with PA or stimulated with zymosan bioparticles. Autophagy was tested by fluorescent microscopy and Western blot for LC3. Phagocytosis and killing efficiency were assessed by plate count assay, flow cytometry or immunofluorescent staining. Phagocytic receptor expression, ROS generation and NO production were examined by PCR, flow cytometry and Griess reaction, respectively.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">PA infection induced autophagy activation in both mouse and human macrophages. Induction of autophagy by rapamycin or starvation significantly inhibited PA internalization by downregulating phagocytosis receptor expression, and suppressed intracellular killing of PA via reducing ROS and NO production in macrophages. While knockdown of autophagy molecules ATG7 or Beclin1 enhanced macrophage-mediated phagocytosis and intracellular killing of PA. Additionally, confocal microscopy data showed that induction of autophagy reduced the number of phagosomes and phagolysosomes in macrophages after stimulation with zymosan bioparticles.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Our study suggested that PA promotes autophagy to suppress macrophage-mediated bacterial phagocytosis and intracellular killing. These insights demonstrated a novel immune evasion mechanism employed by PA, which may provide potential therapeutic strategies of PA infectious diseases.</AbstractText>
<CopyrightInformation>Copyright © 2016 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Yongjian</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Dandan</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Department of Clinical Laboratory, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 243000, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Kang</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China; Division of Clinical Laboratory, Zhongshan Hospital of Sun Yat-sen University, Zhongshan 528403, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yang</LastName>
<ForeName>Kun</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Huang</LastName>
<ForeName>Xi</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Yuanqing</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: zyqsinap@gmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wu</LastName>
<ForeName>Minhao</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Immunology, Institute of Tuberculosis Control, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Key Laboratory of Tropical Diseases Control (Sun Yat-sen University), Ministry of Education, Guangzhou 510080, China. Electronic address: wuminhao@mail.sysu.edu.cn.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>06</Month>
<Day>11</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Int Immunopharmacol</MedlineTA>
<NlmUniqueID>100965259</NlmUniqueID>
<ISSNLinking>1567-5769</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071186">Beclin-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber>
<NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 6.2.1.45</RegistryNumber>
<NameOfSubstance UI="D000071193">Autophagy-Related Protein 7</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071193" MajorTopicYN="N">Autophagy-Related Protein 7</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057131" MajorTopicYN="Y">Immune Evasion</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007113" MajorTopicYN="N">Immunity, Innate</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011552" MajorTopicYN="N">Pseudomonas Infections</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011550" MajorTopicYN="N">Pseudomonas aeruginosa</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000067996" MajorTopicYN="N">RAW 264.7 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="N">RNA, Small Interfering</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Autophagy</Keyword>
<Keyword MajorTopicYN="N">Bacterial killing</Keyword>
<Keyword MajorTopicYN="N">Macrophages</Keyword>
<Keyword MajorTopicYN="N">Phagocytosis</Keyword>
<Keyword MajorTopicYN="N">Pseudomonas aeruginosa</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year>
<Month>02</Month>
<Day>24</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2016</Year>
<Month>04</Month>
<Day>12</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>04</Month>
<Day>29</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2016</Year>
<Month>6</Month>
<Day>14</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2016</Year>
<Month>6</Month>
<Day>14</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2017</Year>
<Month>4</Month>
<Day>7</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">27295610</ArticleId>
<ArticleId IdType="pii">S1567-5769(16)30187-4</ArticleId>
<ArticleId IdType="doi">10.1016/j.intimp.2016.04.044</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<region><li>Guangdong</li>
</region>
<settlement><li>Jiangmen</li>
</settlement>
</list>
<tree><country name="République populaire de Chine"><region name="Guangdong"><name sortKey="Wu, Yongjian" sort="Wu, Yongjian" uniqKey="Wu Y" first="Yongjian" last="Wu">Yongjian Wu</name>
</region>
<name sortKey="Chen, Kang" sort="Chen, Kang" uniqKey="Chen K" first="Kang" last="Chen">Kang Chen</name>
<name sortKey="Huang, Xi" sort="Huang, Xi" uniqKey="Huang X" first="Xi" last="Huang">Xi Huang</name>
<name sortKey="Li, Dandan" sort="Li, Dandan" uniqKey="Li D" first="Dandan" last="Li">Dandan Li</name>
<name sortKey="Wang, Yi" sort="Wang, Yi" uniqKey="Wang Y" first="Yi" last="Wang">Yi Wang</name>
<name sortKey="Wu, Minhao" sort="Wu, Minhao" uniqKey="Wu M" first="Minhao" last="Wu">Minhao Wu</name>
<name sortKey="Yang, Kun" sort="Yang, Kun" uniqKey="Yang K" first="Kun" last="Yang">Kun Yang</name>
<name sortKey="Zhang, Yuanqing" sort="Zhang, Yuanqing" uniqKey="Zhang Y" first="Yuanqing" last="Zhang">Yuanqing Zhang</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000A39 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000A39 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:27295610
   |texte=   Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:27295610" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1

This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020

	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.

Pseudomonas aeruginosa promotes autophagy to suppress macrophage-mediated bacterial eradication.

Source :

Descripteurs français

English descriptors

Abstract

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

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki