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About:
Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo
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schema:ScholarlyArticle
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wasabi.inria.fr
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Type:
Academic Article
research paper
schema:ScholarlyArticle
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type
Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo
Creator
Liu, Yan
Walker, David
Hwang, Seungmin
Wang, Jin
Bechelli, Jeremy
Bender, Sean
Fang, Rong
Garg, Nisha
Smalley, Claire
Vergara, Leoncio
Zhang, William
Popov, Vsevolod
Buzhdygan, Tetyana
Source
PMC
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.
has issue date
2018-12-19
(
xsd:dateTime
)
bibo:doi
10.1128/iai.00651-18
bibo:pmid
30297526
has license
cc-by
sha1sum (hex)
c9c34b0ef9eacdf1bce00a71e1ff612479c3f004
schema:url
https://doi.org/10.1128/iai.00651-18
resource representing a document's title
Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo
has PubMed Central identifier
PMC6300621
has PubMed identifier
30297526
schema:publication
Infect Immun
resource representing a document's body
covid:c9c34b0ef9eacdf1bce00a71e1ff612479c3f004#body_text
is
schema:about
of
named entity 'POORLY'
covid:arg/c9c34b0ef9eacdf1bce00a71e1ff612479c3f004
named entity 'COMPETENT'
named entity 'INCREASED'
named entity 'INITIAL'
named entity 'INFECTION'
named entity 'FORM'
named entity 'RICKETTSIA AUSTRALIS INFECTION'
named entity 'MICE'
named entity 'MICROVASCULAR'
named entity 'INDUCED'
named entity 'AUSTRALIS'
named entity '90%'
named entity 'DATA'
named entity 'DEMONSTRATED'
named entity 'RESULTS'
named entity 'TREATMENT'
named entity 'FLUX'
named entity 'THEIR'
named entity 'LIFE-THREATENING INFECTIONS'
named entity 'VACUOLES'
named entity 'ASSOCIATION'
named entity 'MEMBRANE'
named entity 'ESTABLISHING'
named entity 'DEFICIENT'
named entity 'ONE OF'
named entity 'LIGHT CHAIN'
named entity 'ANALYSIS'
named entity 'MOUSE'
named entity 'HOW'
named entity 'ATG5'
named entity 'MACROPHAGES'
named entity 'PRODUCTION'
named entity 'FREE'
named entity 'TURNOVER'
named entity 'RAPAMYCIN'
named entity 'GREATER'
named entity 'MACROPHAGES'
named entity 'AUTOPHAGY'
named entity 'CONCENTRATION OF'
named entity 'COLOCALIZATION'
named entity 'HUMANS'
named entity 'ENDOTHELIAL CELLS'
named entity 'RICKETTSIAE'
named entity 'DOUBLE'
named entity 'UNDERSTOOD'
named entity 'ATG5'
named entity 'UNTREATED'
named entity 'HERE'
named entity 'EXOGENOUS'
named entity 'RICKETTSIA AUSTRALIS'
named entity 'INFECTED'
named entity 'IL-1'
named entity 'RECOMBINANT'
named entity 'CONCENTRATIONS'
named entity 'PORTION'
named entity 'TAKEN'
named entity 'BUT'
named entity 'BONE MARROW'
named entity 'LYZ'
named entity 'THESE'
named entity 'ABOLISHED'
named entity 'CRE'
named entity 'LC3'
named entity 'SUPPRESSED'
named entity 'TARGETS'
named entity 'INTERLEUKIN-1'
named entity 'OUR'
named entity 'SERUM'
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