Effect of GPR31-signaling on gene expression in LysoDCs during Listeria monocytogenes infection.
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ABSTRACT:
PROVIDER: PRJNA1254235 | ENA |
REPOSITORIES: ENA
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Project description:GPR31 signaling induced dendrite protrusion of lysozyme-expressing dendritic cells (LysoDCs) into basolateral pockets of M cells. To investigate the effect of GPR31 signaling on LysoDC function during infection, we analyzed the gene expression profile of LysoDCs from WT and Gpr31b-deficient mice at 2 days after L. monocytogenes infection.
2025-08-01 | GSE295342 | GEO
Project description:RNASeq of the human epithelial cell line LoVo following Listeria monocytogenes infection
2015-09-15 | E-MTAB-3649 | biostudies-arrayexpress
Project description:Several Toll-like receptors are activated by Listeria monocytogenes infection, resulting in the activation of MyD88 dependent signaling pathway. However, the negative role of MyD88 in gene expresson is unclear. To address this, we performed microarray analysis of mRNAs from WT or MyD88-/- peritoneal macrophages infected with Listeria monocytogenes.
2014-06-29 | GSE52115 | GEO
Project description:ISG15 is primarily documented as an interferon-stimulated, ubiquitin-like protein (ubl), which has anti-viral activity. Although ISG15 was the founding member of the ubl protein family, very little is known about its function. We have found that ISG15 expression in non-phagocytic cells is dramatically induced upon Listeria infection and that surprisingly this induction can be Type I Interferon independent. Listeria-mediated ISG15 induction depends on the cytosolic surveillance pathway, which senses bacterial DNA and signals through STING, TBK1, IRF3 and IRF7. Most importantly, we observed that ISG15 expression restricts Listeria infection both in vitro and in vivo. We then made use of Stable Isotope Labeling in tissue culture (SILAC) to identify the ISGylated proteins that could be responsible for the ISG15-mediated protective effect. Our SILAC analysis revealed that overexpression of ISG15 leads to a striking ISGylation of integral membrane proteins of the endoplasmic reticulum and Golgi apparatus, which correlates with increased canonical secretion of cytokines. Taken together, our data reveal a previously uncharacterized signaling pathway that restricts Listeria infection and acts via ISGylation, reinforcing the view that ISG15 is a key component of the innate immune arsenal of the mammalian host.
2017-03-29 | MSV000080750 | MassIVE
Project description:Time course study of the mouse infection by comparing the genomic transcriptional patterns of Listeria monocytogenes EGDe grown under laboratory conditions (exponential growth phase) with that of in vivo-grown bacteria (in mouse spleens) over three days of infection.
2009-05-29 | GSE13057 | GEO
Project description:ISG15 is primarily documented as an interferon-stimulated, ubiquitin-like protein (ubl), which has anti-viral activity. Although ISG15 was the founding member of the ubl protein family, very little is known about its function. We have found that ISG15 expression in non-phagocytic cells is dramatically induced upon Listeria infection and that surprisingly this induction can be Type I Interferon independent. Listeria-mediated ISG15 induction depends on the cytosolic surveillance pathway, which senses bacterial DNA and signals through STING, TBK1, IRF3 and IRF7. Most importantly, we observed that ISG15 expression restricts Listeria infection both in vitro and in vivo. We then made use of Stable Isotope Labeling in tissue culture (SILAC) to identify the ISGylated proteins that could be responsible for the ISG15-mediated protective effect. Our SILAC analysis revealed that overexpression of ISG15 leads to a striking ISGylation of integral membrane proteins of the endoplasmic reticulum and Golgi apparatus, which correlates with increased canonical secretion of cytokines. Taken together, our data reveal a previously uncharacterized signaling pathway that restricts Listeria infection and acts via ISGylation, reinforcing the view that ISG15 is a key component of the innate immune arsenal of the mammalian host.
2015-07-24 | PXD001805 | Pride
Project description:Time course study of the mouse infection by comparing the genomic transcriptional patterns of Listeria monocytogenes EGDe grown under laboratory conditions (exponential growth phase) with that of in vivo-grown bacteria (in mouse spleens) over three days of infection. Time course study of the mouse infection by comparing the genomic transcriptional patterns of Listeria monocytogenes EGDe grown under laboratory conditions (exponential growth phase) with that of in vivo-grown bacteria (in mouse spleens) over three days of infection.
2010-06-25 | E-GEOD-13057 | biostudies-arrayexpress
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
Project description:ISG15 counteracts Listeria monocytogenes infection
| PRJEB9655 | ENA
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