About: Atg5 Supports Rickettsia australis Infection in Macrophages In Vitro and In Vivo

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
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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