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Misregulation of the broad-range phospholipase C activity increases the susceptibility of Listeria monocytogenes to intracellular killing by neutrophils

ABSTRACT: Listeria monocytogenes is a facultative intracellular bacterial pathogen that tightly regulates the activities of various virulence factors during infection. A mutant strain (the plcBΔpro mutant) that has lost the ability to control the activity of a phospholipase C (PC-PLC) is attenuated a hundred fold in mice. This attenuation is not due to a lack of bacterial fitness, but appears to result from a modified host response to infection. The transcriptomic pattern of immunerelated genes in infected macrophages indicated no differential response to wild-type L. monocytogenes vs the plcBΔpro mutant.

ORGANISM(S): Mus musculus

PROVIDER: GSE49820 | GEO | 2013/08/14

SECONDARY ACCESSION(S): PRJNA215020

REPOSITORIES: GEO

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Misregulation of the broad-range phospholipase C activity increases the susceptibility of Listeria monocytogenes to intracellular killing by neutrophils

Project description:Listeria monocytogenes is a facultative intracellular bacterial pathogen that tightly regulates the activities of various virulence factors during infection. A mutant strain (the plcBM-NM-^Tpro mutant) that has lost the ability to control the activity of a phospholipase C (PC-PLC) is attenuated a hundred fold in mice. This attenuation is not due to a lack of bacterial fitness, but appears to result from a modified host response to infection. The transcriptomic pattern of immunerelated genes in infected macrophages indicated no differential response to wild-type L. monocytogenes vs the plcBM-NM-^Tpro mutant. Cultures of bone marrow derived macrophages from BALB/c were infected with either wild type or mutant L. monocytogens for 3, 6, or 9 hrs. The macrophages were then collected and RNA isolated for microarray analysis of gene expression.

2013-08-14 | E-GEOD-49820 | biostudies-arrayexpress

Expression analysis with Phospholipase C over expression

2012-04-24 | GSE35677 | GEO

Expression analysis with Phospholipase C over expression

2012-09-01 | GSE35745 | GEO

Listeria monocytogenes Transcriptome with RNA-Seq

Project description:The stationary phase stress response transcriptome of the human bacterial pathogen Listeria monocytogenes was defined using RNA sequencing (RNA-Seq) with the Illumina Genome Analyzer. Specifically, bacterial transcriptomes were compared between stationary phase cells of L. monocytogenes 10403S and an otherwise isogenic DsigB mutant, which does not express the alternative sigma factor σB, a major regulator of genes contributing to stress response. Keywords: Transcriptome and differential expression analyses

2010-01-05 | GSE15651 | GEO

Expression analysis with Phospholipase C over expression

Project description:The regulation of phospholipid biosynthesis in Saccharomyces cerevisiae through cis-acting upstream activating sequence inositol (UASino) and trans-acting elements, such as the INO2-INO4 complex and OPI1 by inositol supplementation in growth is thoroughly studied. In this study, we provide evidence for the regulation of lipid biosynthesis by phosphatidylinositol-specific phospholipase C (PLC) through UASino and two trans-acting elements. Gene expression analysis and radiolabelling experiments demonstrated that the overexpression of rice PLC in yeast cells altered phospholipid biosynthesis at the levels of transcriptional and enzyme activity. There are two biological replicates two hour and five hour induction with galactose. The genome wide expression of Saccharomyces cerevisiae strain BY4741 harbouring rPLC-pYES2 and a vectro control (pYES2) were compare with each other. (Agilent Gene Expression Saccharomyces cerevisiae 8x15k array AMADID: 016333)

2012-04-23 | E-GEOD-35677 | biostudies-arrayexpress

Expression analysis with Phospholipase C over expression

Project description:The regulation of phospholipid biosynthesis in Saccharomyces cerevisiae through cis-acting upstream activating sequence inositol (UASino) and trans-acting elements, such as the INO2-INO4 complex and OPI1 by inositol supplementation in growth is thoroughly studied. In this study, we provide evidence for the regulation of lipid biosynthesis by phosphatidylinositol-specific phospholipase C (PLC) through UASino and two trans-acting elements. Gene expression analysis and radiolabelling experiments demonstrated that the overexpression of rice PLC in yeast cells altered phospholipid biosynthesis at the levels of transcriptional and enzyme activity. There are two biological replicates two hour and five hour induction with galactose. The genome wide expression of Saccharomyces cerevisiae strain BY4741 harbouring (rice) rPLC-pYES2 and a vectro control (pYES2) were compare with each other. (Agilent Gene Expression Saccharomyces cerevisiae 8x15k array AMADID: 016333)

2012-09-01 | E-GEOD-35745 | biostudies-arrayexpress

Intracellular transcription by multiple Listeria monocytogenes strains

Project description:These studies were designed to examine the transcription of Listeria monocytogenes strains 10403S and LO28 during intracellular replication in mammalian macrophages. Duplicate WT Listeria monocytogenes (strains 10403S and LO28) were used to infect mouse bone marrow-derived macrophages (BMMs). Bacterial RNA was harvested at 4 hours post-infection.

2011-12-02 | E-GEOD-34083 | biostudies-arrayexpress

Listeria monocytogenes Transcriptome with RNA-Seq

Project description:The stationary phase stress response transcriptome of the human bacterial pathogen Listeria monocytogenes was defined using RNA sequencing (RNA-Seq) with the Illumina Genome Analyzer. Specifically, bacterial transcriptomes were compared between stationary phase cells of L. monocytogenes 10403S and an otherwise isogenic DsigB mutant, which does not express the alternative sigma factor M-OM-^CB, a major regulator of genes contributing to stress response. Keywords: Transcriptome and differential expression analyses a laboratory strain, 10403S and its otherwise isogenic mutant lacking sigB were analyzed. Two replicates of each strain were analyzed for a total of 4 runs

2010-01-05 | E-GEOD-15651 | biostudies-arrayexpress

Listeria monocytogenes exploits the MICOS complex subunit Mic10 to promote mitochondrial fragmentation and cellular infection

Project description:Mitochondrial function adapts to cellular demands and is affected by the ability of the organelle to undergo fusion and fission in response to physiological and non-physiological cues. We previously showed that infection with the human bacterial pathogen Listeria monocytogenes elicits transient mitochondrial fission and a drop in mitochondrial -dependent energy production through a mechanism requiring the bacterial pore-forming toxin listeriolysin O (LLO). Here, we performed quantitative mitochondrial proteomics to search for host factors involved in L. monocytogenes-induced mitochondrial fission. We found that Mic10, a critical component of the mitochondrial contact site and cristae organizing system (MICOS) complex, is significantly enriched in mitochondria isolated from cells infected with wild-type but not with LLO-deficient L. monocytogenes. Increased mitochondrial Mic10 levels did not correlate with upregulated transcription, suggesting a post-transcriptional regulation. We showed that Mic10 is necessary for L. monocytogenes-induced mitochondrial network fragmentation, and that it contributes to L. monocytogenes cellular infection independently of MICOS proteins Mic13, Mic26 and Mic27. Together, L. monocytogenes infection allowed us to uncover a role for Mic10 in mitochondrial fission.

2020-02-17 | PXD014667 | Pride

Listeria infection in hepatocytes

Project description:Listeria monocytogenes causes severe foodborne illness in pregnant women and immunocompromised individuals. After the intestinal phase of infection, the liver plays a central role in the clearance of this pathogen through its important functions in immunity. However, recent evidence suggests that subpopulations of L. monocytogenes may escape eradication after prolonged infection of hepatocytes, by entering a persistence phase in vacuoles. Here, we examine whether this long-term infection alters hepatocyte defense pathways, which may be instrumental for bacterial persistence. We first established models of Listeria infection in human hepatocyte cell lines HepG2 and Huh7 and in primary mouse hepatocytes (PMH). In these cells, Listeria efficiently enters the persistence stage after a 3-day infection, while inducing a type I (PMH) or type I/III (HepG2) or no (Huh7) interferon response. RNA-seq analysis identified a common signature of long-term Listeria infection on the hepatocyte transcriptome, characterized by overexpression of a set of genes involved in antiviral immunity and under-expression of many acute phase protein (APP) genes, particularly involved in the complement and coagulation systems. The decrease in APP transcript amounts correlated with lower protein abundance in the secretome of infected cells, as shown by proteomics, and also occurred in the presence of APP inducers (IL-6 or IL-1b). The results also suggest that long-term Listeria infection affects lipid metabolism pathways. Collectively, these results reveal that long-term infection with L. monocytogenes profoundly deregulates the innate immune functions of hepatocytes, which could generate an environment favorable to the establishment of persistent infection.

2021-11-02 | PXD027154 | Pride

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