ABSTRACT: Transcriptome (Affymetrix arrays) of HepG2 cells uninfected (Cont) or infected with the pathogen Listeria monocytogenes (Inf) for 24 or 72 hours.
Project description:Transcriptome (Affymetrix arrays) and Methylome of HepG2 cells uninfected (Cont) or infected with the pathogen Listeria monocytogenes (Inf)
Project description:Comparisons of gene expression profiles of human hepatocytes (HepG2) infected or not by the bacterium Listeria monocytogenes (strain EGD-e expressing GFP) for 24 or 72 hours and use of Affymetrix microarrays. Samples noted S72h have been sorted by FACS.
Project description:Comparisons of gene expression profiles of human hepatocytes (HepG2) infected or not by the bacterium Listeria monocytogenes (strain EGD-e) for 72 hours and analysed by RNA-seq
Project description:Comparisons of gene expression profiles PMH infected or not by the bacterium Listeria monocytogenes (strain 10403S) for 72 hours and analysed by RNA-seq
Project description:Comparisons of gene expression profiles of human hepatocytes (Huh7) infected or not by the bacterium Listeria monocytogenes (strain EGD-e) for 72 hours and analysed by RNA-seq
Project description:Methylome of of HepG2 cells uninfected ("Cont") or infected with the pathogen Listeria monocytogenes ("Inf") by Methyl-binding domain-sequencing (MBD-Seq/MethylCap-Seq)
Project description:We report the partial methylome (CG-rich regions) of human hepatocytes (HepG2) infected or not by the bacterium Listeria monocytogenes
Project description:IL-17A and IL-22 induced several inflammation-induced genes and anti-microbial molecules including Pla2g2a and Lcn2 on HepG2 cells when the cells were treated with the cytokines before Listeria monocytogenes infection. HepG2 cells were treated with 50 ng/ml IL-17A and 10 ng/ml IL-22 before L. monocytogenes in vitro infection at MOI 10. Reference cells were not treated with the cytokines before the infection. Two independent experiments were carried out.
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.
Project description:IL-17A and IL-22 induced several inflammation-induced genes and anti-microbial molecules including Pla2g2a and Lcn2 on HepG2 cells when the cells were treated with the cytokines before Listeria monocytogenes infection.
