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NLRP3 and mTOR Reciprocally Regulate Macrophage Phagolysosome Formation and Acidification Against Vibrio vulnificus Infection.

Identifieur interne : 000078 ( Main/Exploration ); précédent : 000077; suivant : 000079

NLRP3 and mTOR Reciprocally Regulate Macrophage Phagolysosome Formation and Acidification Against Vibrio vulnificus Infection.

Auteurs : Xian-Hui Huang [République populaire de Chine] ; Yao Ma [République populaire de Chine] ; Meng-Meng Zheng [République populaire de Chine] ; Na Chen [République populaire de Chine] ; Mei-Na Hu [République populaire de Chine] ; Liu-Ying Wu [République populaire de Chine] ; Yi Zheng [République populaire de Chine] ; Yong-Liang Lou [République populaire de Chine] ; Dan-Li Xie [République populaire de Chine]

Source :

RBID : pubmed:33117816

Abstract

The marine bacterium Vibrio vulnificus causes potentially fatal bloodstream infections, typically in patients with chronic liver diseases. The inflammatory response and anti-bacterial function of phagocytes are crucial for limiting bacterial infection in the human hosts. How V. vulnificus affects macrophages after phagocytosis is unclear. In this report, we found that the bactericidal activity of macrophages to internalize V. vulnificus was dependent on mammalian target of rapamycin (mTOR) and NOD-like receptor (NLR) family pyrin domain containing 3 (NLRP3) interaction. Additionally, the NLRP3 expression was dependent on mTORC1 activation. Inhibited mTORC1 or absence of NLRP3 in macrophages impaired V. vulnificus-induced phagosome acidification and phagolysosome formation, leading to a reduction of intracellular bacterial clearance. mTORC1 signaling overactivation could increase NLRP3 expression and restore insufficient phagosome acidification. Together, these findings indicate that the intracellular bactericidal activity of macrophages responding to V. vulnificus infection is tightly controlled by the crosstalk of NLRP3 and mTOR and provide critical insight into the host bactericidal activity basis of clearance of V. vulnificus through lyso/phagosome.

DOI: 10.3389/fcell.2020.587961
PubMed: 33117816
PubMed Central: PMC7578225


Affiliations:


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<div type="abstract" xml:lang="en">The marine bacterium
<i>Vibrio vulnificus</i>
causes potentially fatal bloodstream infections, typically in patients with chronic liver diseases. The inflammatory response and anti-bacterial function of phagocytes are crucial for limiting bacterial infection in the human hosts. How
<i>V. vulnificus</i>
affects macrophages after phagocytosis is unclear. In this report, we found that the bactericidal activity of macrophages to internalize
<i>V. vulnificus</i>
was dependent on mammalian target of rapamycin (mTOR) and NOD-like receptor (NLR) family pyrin domain containing 3 (NLRP3) interaction. Additionally, the NLRP3 expression was dependent on mTORC1 activation. Inhibited mTORC1 or absence of NLRP3 in macrophages impaired
<i>V. vulnificus</i>
-induced phagosome acidification and phagolysosome formation, leading to a reduction of intracellular bacterial clearance. mTORC1 signaling overactivation could increase NLRP3 expression and restore insufficient phagosome acidification. Together, these findings indicate that the intracellular bactericidal activity of macrophages responding to
<i>V. vulnificus</i>
infection is tightly controlled by the crosstalk of NLRP3 and mTOR and provide critical insight into the host bactericidal activity basis of clearance of
<i>V. vulnificus</i>
through lyso/phagosome.</div>
</front>
</TEI>
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<MedlineCitation Status="PubMed-not-MEDLINE" Owner="NLM">
<PMID Version="1">33117816</PMID>
<DateRevised>
<Year>2020</Year>
<Month>10</Month>
<Day>30</Day>
</DateRevised>
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<Journal>
<ISSN IssnType="Print">2296-634X</ISSN>
<JournalIssue CitedMedium="Print">
<Volume>8</Volume>
<PubDate>
<Year>2020</Year>
</PubDate>
</JournalIssue>
<Title>Frontiers in cell and developmental biology</Title>
<ISOAbbreviation>Front Cell Dev Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>NLRP3 and mTOR Reciprocally Regulate Macrophage Phagolysosome Formation and Acidification Against
<i>Vibrio vulnificus</i>
Infection.</ArticleTitle>
<Pagination>
<MedlinePgn>587961</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.3389/fcell.2020.587961</ELocationID>
<Abstract>
<AbstractText>The marine bacterium
<i>Vibrio vulnificus</i>
causes potentially fatal bloodstream infections, typically in patients with chronic liver diseases. The inflammatory response and anti-bacterial function of phagocytes are crucial for limiting bacterial infection in the human hosts. How
<i>V. vulnificus</i>
affects macrophages after phagocytosis is unclear. In this report, we found that the bactericidal activity of macrophages to internalize
<i>V. vulnificus</i>
was dependent on mammalian target of rapamycin (mTOR) and NOD-like receptor (NLR) family pyrin domain containing 3 (NLRP3) interaction. Additionally, the NLRP3 expression was dependent on mTORC1 activation. Inhibited mTORC1 or absence of NLRP3 in macrophages impaired
<i>V. vulnificus</i>
-induced phagosome acidification and phagolysosome formation, leading to a reduction of intracellular bacterial clearance. mTORC1 signaling overactivation could increase NLRP3 expression and restore insufficient phagosome acidification. Together, these findings indicate that the intracellular bactericidal activity of macrophages responding to
<i>V. vulnificus</i>
infection is tightly controlled by the crosstalk of NLRP3 and mTOR and provide critical insight into the host bactericidal activity basis of clearance of
<i>V. vulnificus</i>
through lyso/phagosome.</AbstractText>
<CopyrightInformation>Copyright © 2020 Huang, Ma, Zheng, Chen, Hu, Wu, Zheng, Lou and Xie.</CopyrightInformation>
</Abstract>
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<Author ValidYN="Y">
<LastName>Huang</LastName>
<ForeName>Xian-Hui</ForeName>
<Initials>XH</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Wenzhou Key Laboratory of Sanitary Microbiology, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Ma</LastName>
<ForeName>Yao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zheng</LastName>
<ForeName>Meng-Meng</ForeName>
<Initials>MM</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Chen</LastName>
<ForeName>Na</ForeName>
<Initials>N</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Hu</LastName>
<ForeName>Mei-Na</ForeName>
<Initials>MN</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Wu</LastName>
<ForeName>Liu-Ying</ForeName>
<Initials>LY</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zheng</LastName>
<ForeName>Yi</ForeName>
<Initials>Y</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Wenzhou Key Laboratory of Sanitary Microbiology, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Lou</LastName>
<ForeName>Yong-Liang</ForeName>
<Initials>YL</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Wenzhou Key Laboratory of Sanitary Microbiology, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Xie</LastName>
<ForeName>Dan-Li</ForeName>
<Initials>DL</Initials>
<AffiliationInfo>
<Affiliation>Department of Microbiology and Immunology, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Key Laboratory of Laboratory Medicine, Ministry of Education of China, Wenzhou, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo>
<Affiliation>Wenzhou Key Laboratory of Sanitary Microbiology, Wenzhou, China.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
<PublicationTypeList>
<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic">
<Year>2020</Year>
<Month>10</Month>
<Day>08</Day>
</ArticleDate>
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<Country>Switzerland</Country>
<MedlineTA>Front Cell Dev Biol</MedlineTA>
<NlmUniqueID>101630250</NlmUniqueID>
<ISSNLinking>2296-634X</ISSNLinking>
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<Keyword MajorTopicYN="N">NLRP3</Keyword>
<Keyword MajorTopicYN="N">Vibrio vulnificus</Keyword>
<Keyword MajorTopicYN="N">acidification</Keyword>
<Keyword MajorTopicYN="N">bactericidal activity</Keyword>
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</record>

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EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000078 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000078 | 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:33117816
   |texte=   NLRP3 and mTOR Reciprocally Regulate Macrophage Phagolysosome Formation and Acidification Against Vibrio vulnificus Infection.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:33117816" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1 

Wicri

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