RapamycinFungusV1, Main, Exploration, bibRecord, 000409

Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo.

Identifieur interne : 000409 ( Main/Exploration ); précédent : 000408; suivant : 000410

Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo.

Auteurs : Jeremy Bechelli [États-Unis] ; Leoncio Vergara [États-Unis] ; Claire Smalley [États-Unis] ; Tetyana P. Buzhdygan [États-Unis] ; Sean Bender [États-Unis] ; William Zhang [États-Unis] ; Yan Liu [États-Unis] ; Vsevolod L. Popov [États-Unis] ; Jin Wang [États-Unis] ; Nisha Garg [États-Unis] ; Seungmin Hwang [États-Unis] ; David H. Walker [États-Unis] ; Rong Fang [États-Unis]

Source :

Infection and immunity [ 1098-5522 ] ; 2019.

RBID : pubmed:30297526

Descripteurs français

KwdFr :
- Animaux (MeSH), Cellules cultivées (MeSH), Femelle (MeSH), Interactions hôte-pathogène (MeSH), Interleukine-1 bêta (métabolisme), Macrophages (microbiologie), Macrophages (métabolisme), Protéine-5 associée à l'autophagie (métabolisme), Rickettsia (croissance et développement), Rickettsiose du groupe des fièvres boutonneuses (MeSH), Souris de lignée C57BL (MeSH).
MESH :
- croissance et développement : Rickettsia.
- microbiologie : Macrophages.
- métabolisme : Interleukine-1 bêta, Macrophages, Protéine-5 associée à l'autophagie.
- Animaux, Cellules cultivées, Femelle, Interactions hôte-pathogène, Rickettsiose du groupe des fièvres boutonneuses, Souris de lignée C57BL.

English descriptors

KwdEn :
- Animals (MeSH), Autophagy-Related Protein 5 (metabolism), Cells, Cultured (MeSH), Female (MeSH), Host-Pathogen Interactions (MeSH), Interleukin-1beta (metabolism), Macrophages (metabolism), Macrophages (microbiology), Mice, Inbred C57BL (MeSH), Rickettsia (growth & development), Spotted Fever Group Rickettsiosis (MeSH).
MESH :
- chemical , metabolism : Autophagy-Related Protein 5, Interleukin-1beta.
- growth & development : Rickettsia.
- metabolism : Macrophages.
- microbiology : Macrophages.
- Animals, Cells, Cultured, Female, Host-Pathogen Interactions, Mice, Inbred C57BL, Spotted Fever Group Rickettsiosis.

Abstract

Rickettsiae can cause life-threatening infections in humans. Macrophages are one of the initial targets for rickettsiae after inoculation by ticks. However, it remains poorly understood how rickettsiae remain free in macrophages prior to establishing their infection in microvascular endothelial cells. Here, we demonstrated that the concentration of Rickettsia australis was significantly greater in infected tissues of Atg5^flox/flox mice than in the counterparts of Atg5^flox/flox Lyz-Cre mice, in association with a reduced level of interleukin-1β (IL-1β) in serum. The greater concentration of R. australis in Atg5^flox/flox bone marrow-derived macrophages (BMMs) than in Atg5^flox/flox Lyz-Cre BMMs in vitro was abolished by exogenous treatment with recombinant IL-1β. Rickettsia australis induced significantly increased levels of light chain 3 (LC3) form II (LC3-II) and LC3 puncta in Atg5-competent BMMs but not in Atg5-deficient BMMs, while no p62 turnover was observed. Further analysis found the colocalization of LC3 with a small portion of R. australis and Rickettsia-containing double-membrane-bound vacuoles in the BMMs of B6 mice. Moreover, treatment with rapamycin significantly increased the concentrations of R. australis in B6 BMMs compared to those in the untreated B6 BMM controls. Taken together, our results demonstrate that Atg5 favors R. australis infection in mouse macrophages in association with a suppressed level of IL-1β production but not active autophagy flux. These data highlight the contribution of Atg5 in macrophages to the pathogenesis of rickettsial diseases.

DOI: 10.1128/IAI.00651-18
PubMed: 30297526
PubMed Central: PMC6300621

Affiliations:

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

to stream Main, to step Corpus: 000441
to stream Main, to step Curation: 000441

Le document en format XML

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 Supports <i>Rickettsia australis</i>
 Infection in Macrophages <i>In Vitro</i>
 and <i>In Vivo</i>
.</title>
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<affiliation wicri:level="2"><nlm:affiliation>Department of Biological Sciences, Sam Houston State University, Huntsville, Texas, USA.</nlm:affiliation>
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<author><name sortKey="Buzhdygan, Tetyana P" sort="Buzhdygan, Tetyana P" uniqKey="Buzhdygan T" first="Tetyana P" last="Buzhdygan">Tetyana P. Buzhdygan</name>
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<author><name sortKey="Popov, Vsevolod L" sort="Popov, Vsevolod L" uniqKey="Popov V" first="Vsevolod L" last="Popov">Vsevolod L. Popov</name>
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<author><name sortKey="Fang, Rong" sort="Fang, Rong" uniqKey="Fang R" first="Rong" last="Fang">Rong Fang</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en"><i>Atg5</i>
 Supports <i>Rickettsia australis</i>
 Infection in Macrophages <i>In Vitro</i>
 and <i>In Vivo</i>
.</title>
<author><name sortKey="Bechelli, Jeremy" sort="Bechelli, Jeremy" uniqKey="Bechelli J" first="Jeremy" last="Bechelli">Jeremy Bechelli</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
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</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Department of Biological Sciences, Sam Houston State University, Huntsville, Texas, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Smalley, Claire" sort="Smalley, Claire" uniqKey="Smalley C" first="Claire" last="Smalley">Claire Smalley</name>
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<author><name sortKey="Buzhdygan, Tetyana P" sort="Buzhdygan, Tetyana P" uniqKey="Buzhdygan T" first="Tetyana P" last="Buzhdygan">Tetyana P. Buzhdygan</name>
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<country xml:lang="fr">États-Unis</country>
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<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
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<author><name sortKey="Bender, Sean" sort="Bender, Sean" uniqKey="Bender S" first="Sean" last="Bender">Sean Bender</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
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<author><name sortKey="Zhang, William" sort="Zhang, William" uniqKey="Zhang W" first="William" last="Zhang">William Zhang</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>High School Student Summer Research Program, University of Texas Medical Branch at Galveston, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
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<author><name sortKey="Liu, Yan" sort="Liu, Yan" uniqKey="Liu Y" first="Yan" last="Liu">Yan Liu</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Popov, Vsevolod L" sort="Popov, Vsevolod L" uniqKey="Popov V" first="Vsevolod L" last="Popov">Vsevolod L. Popov</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wang, Jin" sort="Wang, Jin" uniqKey="Wang J" first="Jin" last="Wang">Jin Wang</name>
<affiliation wicri:level="2"><nlm:affiliation>Immunobiology and Transplant Science Center, Houston Methodist Research Institute, Houston, Texas, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Immunobiology and Transplant Science Center, Houston Methodist Research Institute, Houston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
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<author><name sortKey="Garg, Nisha" sort="Garg, Nisha" uniqKey="Garg N" first="Nisha" last="Garg">Nisha Garg</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
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<author><name sortKey="Hwang, Seungmin" sort="Hwang, Seungmin" uniqKey="Hwang S" first="Seungmin" last="Hwang">Seungmin Hwang</name>
<affiliation wicri:level="4"><nlm:affiliation>Department of Pathology, University of Chicago, Chicago, Illinois, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, University of Chicago, Chicago, Illinois</wicri:regionArea>
<placeName><region type="state">Illinois</region>
<settlement type="city">Chicago</settlement>
</placeName>
<orgName type="university">Université de Chicago</orgName>
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<author><name sortKey="Walker, David H" sort="Walker, David H" uniqKey="Walker D" first="David H" last="Walker">David H. Walker</name>
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<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
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<author><name sortKey="Fang, Rong" sort="Fang, Rong" uniqKey="Fang R" first="Rong" last="Fang">Rong Fang</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Autophagy-Related Protein 5 (metabolism)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Female (MeSH)</term>
<term>Host-Pathogen Interactions (MeSH)</term>
<term>Interleukin-1beta (metabolism)</term>
<term>Macrophages (metabolism)</term>
<term>Macrophages (microbiology)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Rickettsia (growth & development)</term>
<term>Spotted Fever Group Rickettsiosis (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Femelle (MeSH)</term>
<term>Interactions hôte-pathogène (MeSH)</term>
<term>Interleukine-1 bêta (métabolisme)</term>
<term>Macrophages (microbiologie)</term>
<term>Macrophages (métabolisme)</term>
<term>Protéine-5 associée à l'autophagie (métabolisme)</term>
<term>Rickettsia (croissance et développement)</term>
<term>Rickettsiose du groupe des fièvres boutonneuses (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autophagy-Related Protein 5</term>
<term>Interleukin-1beta</term>
</keywords>
<keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Rickettsia</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Rickettsia</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</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>Interleukine-1 bêta</term>
<term>Macrophages</term>
<term>Protéine-5 associée à l'autophagie</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cells, Cultured</term>
<term>Female</term>
<term>Host-Pathogen Interactions</term>
<term>Mice, Inbred C57BL</term>
<term>Spotted Fever Group Rickettsiosis</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules cultivées</term>
<term>Femelle</term>
<term>Interactions hôte-pathogène</term>
<term>Rickettsiose du groupe des fièvres boutonneuses</term>
<term>Souris de lignée C57BL</term>
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</teiHeader>
<front><div type="abstract" xml:lang="en">Rickettsiae can cause life-threatening infections in humans. Macrophages are one of the initial targets for rickettsiae after inoculation by ticks. However, it remains poorly understood how rickettsiae remain free in macrophages prior to establishing their infection in microvascular endothelial cells. Here, we demonstrated that the concentration of <i>Rickettsia australis</i>
 was significantly greater in infected tissues of <i>Atg5<sup>flox/flox</sup>
</i>
 mice than in the counterparts of <i>Atg5<sup>flox/flox</sup>
</i>
 Lyz-<i>Cre</i>
 mice, in association with a reduced level of interleukin-1β (IL-1β) in serum. The greater concentration of <i>R. australis</i>
 in <i>Atg5<sup>flox/flox</sup>
</i>
 bone marrow-derived macrophages (BMMs) than in <i>Atg5<sup>flox/flox</sup>
</i>
 Lyz-<i>Cre</i>
 BMMs <i>in vitro</i>
 was abolished by exogenous treatment with recombinant IL-1β. <i>Rickettsia australis</i>
 induced significantly increased levels of light chain 3 (LC3) form II (LC3-II) and LC3 puncta in <i>Atg5</i>
-competent BMMs but not in <i>Atg5</i>
-deficient BMMs, while no p62 turnover was observed. Further analysis found the colocalization of LC3 with a small portion of <i>R. australis</i>
 and <i>Rickettsia</i>
-containing double-membrane-bound vacuoles in the BMMs of B6 mice. Moreover, treatment with rapamycin significantly increased the concentrations of <i>R. australis</i>
 in B6 BMMs compared to those in the untreated B6 BMM controls. Taken together, our results demonstrate that <i>Atg5</i>
 favors <i>R. australis</i>
 infection in mouse macrophages in association with a suppressed level of IL-1β production but not active autophagy flux. These data highlight the contribution of <i>Atg5</i>
 in macrophages to the pathogenesis of rickettsial diseases.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30297526</PMID>
<DateCompleted><Year>2019</Year>
<Month>07</Month>
<Day>01</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>03</Month>
<Day>09</Day>
</DateRevised>
<Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1098-5522</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>87</Volume>
<Issue>1</Issue>
<PubDate><Year>2019</Year>
<Month>01</Month>
</PubDate>
</JournalIssue>
<Title>Infection and immunity</Title>
<ISOAbbreviation>Infect Immun</ISOAbbreviation>
</Journal>
<ArticleTitle><i>Atg5</i>
 Supports <i>Rickettsia australis</i>
 Infection in Macrophages <i>In Vitro</i>
 and <i>In Vivo</i>
.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">e00651-18</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1128/IAI.00651-18</ELocationID>
<Abstract><AbstractText>Rickettsiae can cause life-threatening infections in humans. Macrophages are one of the initial targets for rickettsiae after inoculation by ticks. However, it remains poorly understood how rickettsiae remain free in macrophages prior to establishing their infection in microvascular endothelial cells. Here, we demonstrated that the concentration of <i>Rickettsia australis</i>
 was significantly greater in infected tissues of <i>Atg5<sup>flox/flox</sup>
</i>
 mice than in the counterparts of <i>Atg5<sup>flox/flox</sup>
</i>
 Lyz-<i>Cre</i>
 mice, in association with a reduced level of interleukin-1β (IL-1β) in serum. The greater concentration of <i>R. australis</i>
 in <i>Atg5<sup>flox/flox</sup>
</i>
 bone marrow-derived macrophages (BMMs) than in <i>Atg5<sup>flox/flox</sup>
</i>
 Lyz-<i>Cre</i>
 BMMs <i>in vitro</i>
 was abolished by exogenous treatment with recombinant IL-1β. <i>Rickettsia australis</i>
 induced significantly increased levels of light chain 3 (LC3) form II (LC3-II) and LC3 puncta in <i>Atg5</i>
-competent BMMs but not in <i>Atg5</i>
-deficient BMMs, while no p62 turnover was observed. Further analysis found the colocalization of LC3 with a small portion of <i>R. australis</i>
 and <i>Rickettsia</i>
-containing double-membrane-bound vacuoles in the BMMs of B6 mice. Moreover, treatment with rapamycin significantly increased the concentrations of <i>R. australis</i>
 in B6 BMMs compared to those in the untreated B6 BMM controls. Taken together, our results demonstrate that <i>Atg5</i>
 favors <i>R. australis</i>
 infection in mouse macrophages in association with a suppressed level of IL-1β production but not active autophagy flux. These data highlight the contribution of <i>Atg5</i>
 in macrophages to the pathogenesis of rickettsial diseases.</AbstractText>
<CopyrightInformation>Copyright © 2018 Bechelli et al.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bechelli</LastName>
<ForeName>Jeremy</ForeName>
<Initials>J</Initials>
<Identifier Source="ORCID">0000-0002-8786-7795</Identifier>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biological Sciences, Sam Houston State University, Huntsville, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Vergara</LastName>
<ForeName>Leoncio</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Center for Biomedical Engineering, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Smalley</LastName>
<ForeName>Claire</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Buzhdygan</LastName>
<ForeName>Tetyana P</ForeName>
<Initials>TP</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bender</LastName>
<ForeName>Sean</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>William</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>High School Student Summer Research Program, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Yan</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Popov</LastName>
<ForeName>Vsevolod L</ForeName>
<Initials>VL</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Jin</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Immunobiology and Transplant Science Center, Houston Methodist Research Institute, Houston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Garg</LastName>
<ForeName>Nisha</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hwang</LastName>
<ForeName>Seungmin</ForeName>
<Initials>S</Initials>
<Identifier Source="ORCID">0000-0003-0846-5462</Identifier>
<AffiliationInfo><Affiliation>Department of Pathology, University of Chicago, Chicago, Illinois, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Walker</LastName>
<ForeName>David H</ForeName>
<Initials>DH</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fang</LastName>
<ForeName>Rong</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA rofang@utmb.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R21 AI133359</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AI056210</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R21 AI101413</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 AI123221</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>T32 AI060549</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>12</Month>
<Day>19</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Infect Immun</MedlineTA>
<NlmUniqueID>0246127</NlmUniqueID>
<ISSNLinking>0019-9567</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C495773">Atg5 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071187">Autophagy-Related Protein 5</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D053583">Interleukin-1beta</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071187" MajorTopicYN="N">Autophagy-Related Protein 5</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="Y">Host-Pathogen Interactions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053583" MajorTopicYN="N">Interleukin-1beta</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012281" MajorTopicYN="N">Rickettsia</DescriptorName>
<QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000073605" MajorTopicYN="N">Spotted Fever Group Rickettsiosis</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Atg5</Keyword>
<Keyword MajorTopicYN="Y">IL-1β</Keyword>
<Keyword MajorTopicYN="Y">Rickettsia australis</Keyword>
<Keyword MajorTopicYN="Y">autophagosomes</Keyword>
<Keyword MajorTopicYN="Y">mouse macrophages</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>08</Month>
<Day>21</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>09</Month>
<Day>28</Day>
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	Serveur d'exploration sur la rapamycine et les champignons
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Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo.

Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo.

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