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A Bacterial Protein Targets the BAHD1 Chromatin Complex to Stimulate Type III Interferon Response

ABSTRACT: Intracellular pathogens such as Listeria monocytogenes subvert cellular functions through the interaction of bacterial effectors with host components. Here we found that a secreted listerial virulence factor, LntA, could target the chromatin repressor BAHD1 in the host cell nucleus to activate IFN-stimulated genes (ISGs). IFN-λ expression was induced in response to infection of epithelial cells with bacteria lacking LntA; however, the BAHD1-chromatin associated complex repressed downstream ISGs. In contrast, in cells infected with lntA-expressing bacteria, LntA prevented BAHD1 recruitment to ISGs and stimulated their expression. Murine listeriosis decreased in BAHD1+/- mice or when lntA was constitutively expressed. Thus the LntA-BAHD1 interplay may modulate IFN-λ−mediated immune response to control bacterial colonization of the host. In this dataset, we include the expression data obtained following infection of human Lovo cells infected with Listeria bacteria expressing (LntA-V5+) or not (DlntA) the virulence facteur LntA

ORGANISM(S): Homo sapiens

PROVIDER: GSE26414 | GEO | 2011/02/03

SECONDARY ACCESSION(S): PRJNA136789

REPOSITORIES: GEO

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A Bacterial Protein Targets the BAHD1 Chromatin Complex to Stimulate Type III Interferon Response

Project description:Intracellular pathogens such as Listeria monocytogenes subvert cellular functions through the interaction of bacterial effectors with host components. Here we found that a secreted listerial virulence factor, LntA, could target the chromatin repressor BAHD1 in the host cell nucleus to activate IFN-stimulated genes (ISGs). IFN-M-NM-; expression was induced in response to infection of epithelial cells with bacteria lacking LntA; however, the BAHD1-chromatin associated complex repressed downstream ISGs. In contrast, in cells infected with lntA-expressing bacteria, LntA prevented BAHD1 recruitment to ISGs and stimulated their expression. Murine listeriosis decreased in BAHD1+/- mice or when lntA was constitutively expressed. Thus the LntA-BAHD1 interplay may modulate IFN-M-NM-;M-bM-^HM-^Rmediated immune response to control bacterial colonization of the host. In this dataset, we include the expression data obtained following infection of human Lovo cells infected with Listeria bacteria expressing (LntA-V5+) or not (DlntA) the virulence facteur LntA RNA from LoVo cells grown in 6-well plates and infected with either lntAV5+ or lntAM-bM-^@M-^S strains was extracted. Three biological replicates were analyzed for each experimental condition.

2011-02-03 | E-GEOD-26414 | biostudies-arrayexpress

Analysis of transcriptional signatures in response to Listeria monocytogenes infection reveals temporal and strain dependent changes in interferon signalling

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2016-04-01 | E-GEOD-77102 | biostudies-arrayexpress

Analysis of transcriptional signatures in response to Listeria monocytogenes infection reveals temporal and strain dependent changes in interferon signalling

Project description:Listeriosis is an infectious disease caused by the intracellular bacterium Listeria monocytogenes. To control the infection effectively, the host immune response is directed by intercellular signalling molecules called cytokines that are produced by immune cells following sensing of the bacteria. In this study we used gene expression analysis to examine complex immune signalling networks in the blood and tissues of mice infected with L. monocytogenes. We show that a large set of genes are perturbed in both blood and tissue upon infection and that the transcriptional responses in both are enriched for pathways of the immune response. From these data we also observe an important signalling network emerge from a group of cytokines called interferons (IFNs). Previous findings suggest that different IFN family members can determine the balance between successful and impaired immune responses to L. monocytogenes and several other bacterial infections. Using mice deficient for the detrimental ‘type I’ IFN signalling pathway we show that IFN-inducible genes are differentially regulated at different times upon infection but also present at much lower levels in uninfected mice highlighting how dysregulation of this network in the steady state may determine the outcome of this bacterial infection.

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Type I interferon signaling is required for activation of the inflammasome during Francisella infection

Project description:Francisella are pathogenic bacteria whose virulence is linked to their ability to replicate within the host cell cytosol. Entry into the macrophage cytosol activates a host protective multimolecular complex called the inflammasome to release the proinflammatory cytokines IL-1 and IL-18 and trigger caspase-1 dependent cell death. Here we show that cytosolic Francisella induce a type I interferon (IFN) response that is essential for caspase-1 activation, inflammasome mediated cell death, and release of IL-1 and IL-18. Extensive type I IFN dependent cell death resulting in macrophage depletion occurs in vivo during Francisella infection. Type I IFN is also necessary for inflammasome activation in response to cytosolic Listeria but not vacuole localized Salmonella or extracellular ATP. These results show the specific connection between type I IFN signaling and inflammasome activation, two sequential events triggered by recognition of cytosolic bacteria. To our knowledge, this is the first example of positive regulation of inflammasome activation. This connection underscores the importance of cytosolic recognition of pathogens and highlights how multiple innate immunity pathways interact before commitment to critical host responses. Keywords: murine macrophage response to Francisella tularensis subspecies novicida infection We analyzed a series of 18 MEEBO arrays on which were hybed RNA randomly amplified from bone marrow derived macrophages infected or not with WT Francisella tularensis subspecies novicida or a the mglA mutant strain GB2.

2007-05-23 | E-GEOD-7684 | biostudies-arrayexpress

Type I interferon signaling is required for activation of the inflammasome during Francisella infection

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Interferon lambda restricts West Nile virus neuroinvasion by enhancing integrity of the blood-brain barrier

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