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Subversion of host innate immunity by Rickettsia australis via a modified autophagic response in macrophages

ABSTRACT: Subversion of host innate immunity by Rickettsia australis via a modified autophagic response in macrophages

PROVIDER: PRJNA718569 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14108381_1.fastq.gz	Fastqsanger.gz
	SRR14108381_2.fastq.gz	Fastqsanger.gz
	SRR14108382_1.fastq.gz	Fastqsanger.gz
	SRR14108382_2.fastq.gz	Fastqsanger.gz
	SRR14108383_1.fastq.gz	Fastqsanger.gz

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Subversion of host innate immunity by Rickettsia australis via a modified autophagic response in macrophages

Project description:We recently reported that the in vitro and in vivo survival of Rickettsia australis are Atg5-dependent, in association with an inhibited level of anti-rickettsial cytokine, IL-1β. In the present study, we sought to investigate how R. australis interacts with host innate immunity via an Atg5-dependent autophagic response. We found that the serum levels of IFN-γ and G-CSF in R. australis-infected Atg5flox/floxLyz-Cre mice were significantly less compared to Atg5flox/flox mice, accompanied by significantly lower rickettsial loads in tissues with inflammatory cellular infiltrations including neutrophils. R. australis infection differentially regulated a significant number of genes in bone marrow-derived macrophages (BMMs) in an Atg5-depdent fashion as determined by RNA sequencing and Ingenuity Pathway Analysis, including genes in the molecular networks of IL-1 family cytokines and PI3K-Akt-mTOR. The secretion levels of inflammatory cytokines, such as IL-1α, IL-18, TNF-α, and IL-6, by R. australis-infected Atg5flox/floxLyz-Cre BMMs were significantly greater compared to infected Atg5flox/flox BMMs. Interestingly, R. australis significantly increased the levels of phosphorylated mTOR and P70S6K at a time when the autophagic response is induced. Rapamycin treatment nearly abolished the phosphorylated mTOR and P70S6K but did not promote significant autophagic flux during R. australis infection. These results highlight that R. australis modulates an Atg5-dependent autophagic response, which is not sensitive to regulation by mTORC1 signaling in macrophages. Overall, we demonstrate that R. australis counteracts host innate immunity including IL-1β-dependent inflammatory response to support the bacterial survival via an mTORC1-resistant autophagic response in macrophages.

2021-04-06 | GSE171160 | GEO

Rickettsia australis

Project description:Rickettsia australis overview

| PRJNA76089 | ENA

Subversion of Host Innate Immunity by <i>Rickettsia australis via</i> a Modified Autophagic Response in Macrophages.

Project description:We recently reported that the in vitro and in vivo survivals of Rickettsia australis are Atg5-dependent, in association with an inhibited level of anti-rickettsial cytokine, IL-1β. In the present study, we sought to investigate how R. australis interacts with host innate immunity via an Atg5-dependent autophagic response. We found that the serum levels of IFN-γ and G-CSF in R. australis-infected Atg5flox/flox Lyz-Cre mice were significantly less compared to Atg5flox/flox mice, accompanied by significantly lower rickettsial loads in tissues with inflammatory cellular infiltrations including neutrophils. R. australis infection differentially regulated a significant number of genes in bone marrow-derived macrophages (BMMs) in an Atg5-depdent fashion as determined by RNA sequencing and Ingenuity Pathway Analysis, including genes in the molecular networks of IL-1 family cytokines and PI3K-Akt-mTOR. The secretion levels of inflammatory cytokines, such as IL-1α, IL-18, TNF-α, and IL-6, by R. australis-infected Atg5flox/flox Lyz-Cre BMMs were significantly greater compared to infected Atg5flox/flox BMMs. Interestingly, R. australis significantly increased the levels of phosphorylated mTOR and P70S6K at a time when the autophagic response is induced. Rapamycin treatment nearly abolished the phosphorylated mTOR and P70S6K but did not promote significant autophagic flux during R. australis infection. These results highlight that R. australis modulates an Atg5-dependent autophagic response, which is not sensitive to regulation by mTORC1 signaling in macrophages. Overall, we demonstrate that R. australis counteracts host innate immunity including IL-1β-dependent inflammatory response to support the bacterial survival via an mTORC1-resistant autophagic response in macrophages.

| S-EPMC8071864 | biostudies-literature

Rickettsia australis str. Cutlack

Project description:Rickettsia australis str. Cutlack Genome sequencing

| PRJNA75037 | ENA

Rickettsia australis str. Phillips

Project description:Rickettsia australis str. Phillips Genome sequencing and assembly

| PRJNA167984 | ENA

Genomic comparison of virulent Rickettsia rickettsii Sheila Smith and avirulent Rickettsia rickettsii Iowa

Project description:Comparison of gene expression between the virulent Rickettsia rickettsii R strain and avirulent Rickettsia rickettsii Iowa. Keywords: virulent vs avirulent Virulent Rickettsia rickettsii R strain in triplicate was compared to avirulent Rickettsia rickettsii Iowa in triplicate

2010-05-26 | E-GEOD-8041 | biostudies-arrayexpress

Genomic comparison of virulent Rickettsia rickettsii Sheila Smith and avirulent Rickettsia rickettsii Iowa

Project description:Comparison of gene expression between the virulent Rickettsia rickettsii R strain and avirulent Rickettsia rickettsii Iowa. Keywords: virulent vs avirulent

2008-06-04 | GSE8041 | GEO

Toxin-antitoxin of Rickettsia determines fatal addiction of the host cells

Project description:Rickettsia spp. can cause mild to severe human disease. These intracellular bacteria are associated with arthropods, nematodes and trematodes, and usually, are efficiently transmitted transovarially to the progeny of the invertebrate host. We recently demonstrated foreign gene acquisition by lateral gene transfer in Rickettsia genomes. The unexpected presence of laterally transferred toxin-antitoxin (TA) genetic elements (including vapBC) in several Rickettsia genomes has not been connected with the pathogenic process or the host-bacteria relationship. We suspect that vapBC are selfish genetic elements that addict eukaryotic hosts to Rickettsia. We identified a statistical link between the transovarial transmission of Rickettsia in invertebrate hosts and the presence of TA operons, specifically vapBC, in the Rickettsia genome. These TA are neighboring to type IV secretion genes. Tunel assays and whole-genome expression of infected cells showed that antibiotic eradication of TA-containing Rickettsia from the host in cell culture initiates a proapoptotic program. Rickettsia VapC toxins inhibit the growth of transformed Escherichia coli and Saccharomyces cerevisiae. Rickettsia toxin presents in vitro RNase activity. Annexin-V staining and time-lapse video showed that intracytoplasmic injections of VapC toxins in cells cause apoptosis. These data demonstrate that host cells may develop a dependence on Rickettsia spp. expressing the vapBC operon. This would constitute a new evolutionary “mafia strategy” of intracellular bacteria based on host addiction.

2012-05-24 | GSE22072 | GEO

Gene expression of Rickettsia infected green rice leafhopper Nephotettix cincticeps.

Project description:The green rice leafhopper Nephotettix cincticeps have two mutualistic symbiotic bacteria (Candidatus Sulcia muelleri and Candidatus Nasuia deltocephalinicola) in its symbiont special organ bacteriome and are also infected to rickettsia. In order to determine immune challenge is induced or not by rickettsia infection in N. cincticeps, we investigated gene expression between rickettsia-infected and rifampicin treated uninfected N. cincticeps colonies.

2019-08-20 | GSE135973 | GEO

Rickettsia-HUVECs secretome and Rickettsia-mouse plasma proteome

Project description:Proteomics profiling of the secretome of HUVEC cells infected with Rickettsia; Proteomics pprofiling of the plasma proteome of mice infected with Rickettsia.

2019-09-25 | PXD013548 | Pride

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