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Searched keyword : Listeria monocytogenes
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Listeria monocytogenes is a gram positive facultative intracellular foodborne bacterium responsible for serious clinical manifestations including febrile gastroenteritis, meningitis, encephalitis and maternofetal infections in humans and livestock. Intestinal microbiota plays fundamental roles in the resistance to foodborne infections. Intestinal microbiota commensals protect against pathogens by direct antimicrobial activity through production of bacteriocins, competition for nutrients or binding sites, stimulation of epithelial barrier function, immunomodulation and inhibition of virulence factors expression in gastrointestinal pathogens. On the other side, pathogens have developed tools to avoid commensal-mediated resistance to colonization. Thus, the interplay between gut commensals and L. monocytogenes is critical for the infection and the development of the disease. We have identified a Listeria monocytogenes toxin which modifies the intestinal host microbiota and allows Listeria survival in the intestinal content to later invade the intestine and deeper organs.
In the context of the Swiss consortium InfectX (www.infectx.ch), Javier PIZARRO-CERDA previously performed siRNA, microRNA, drug screens and proteomic analyses to investigate signaling pathways modulating invasion of host cells by the bacterial pathogen Listeria monocytogenes. In a first consortium study, based on results from drug and siRNA screens targeting the human kinome, we identified major kinases which up- or down-regulate cell invasion by L. monocytogenes and by 7 additional bacterial and viral pathogens (Rämö et al. 2014). Subsequently, a siRNA genome-wide screen allowed us to revisit and redefine the role of cytoskeletal complexes required for L. monocytogenes cellular invasion and actin-based motility (Kühbacher et al. 2015). Applying a proteomic ‘surfaceome’ analysis, we also revealed that late endosomal compartments are recruited to L. monocytogenes infection foci to promote invasion (Kühbacher et al. Submitted). More recently, we have started the analysis of a microRNA screen which highlights novel gene clusters associated to regulation of phosphoinositide metabolism during L. monocytogenes cell entry (Kühbacher et al. Unpublished Results). These different projects have generated vast amounts of data that have been until now only independently analyzed. However, this information can now be exploited from a systems biology perspective to identify hidden connections between relevant signaling cascades and gene networks which may highlight novel cellular functions exploited by pathogens in the context of infection. The team of Benno SCHWIKOWSKI will perform two types of analysis on the data generated by Javier PIZARRO-CERDA. In both cases, p-values will be aggregated across gene sets using suitable statistical approaches. We will then
- Pathway-based analysis. This type of analysis considers genes in sets that have been recognized to operate together to perform certain biological functions (e.g.,
Listeria monocytogenes is a gram-positive bacterium responsible for the food-borne disease listeriosis. This pathogen can invade and replicate in the cytoplasm of both macrophages and non-professional phagocytes. In order to better characterize the host response to Listeria, we are using microarrays to identify genes and cytokines up or downregulated during infection.
One of the best models for the study of bacteria-host interactions is Listeria monocytogenes. One interesting facet of this bacterium is its ability to modify host chromatin. Recently, we have shown that Listeria causes a drastic deacetylation of histone H3 on lysine 18 (H3K18dc). Interestingly, to impose this modification, Listeria highjacks previously undescribed host machinery: the host protein sirtuin 2 (SIRT2) is relocalized to the nucleus where it causes genes repression during infection. SIRT2 is a NAD-dependent deacetylase that has been implicated in the regulation of complex processes such as aging and cancer. This protein had been mainly studied in the cytoplasm, and although SIRT2 had been show to shuttle between the cytoplasm and the nucleus, the mechanism and its biological role remained unknown. In order to further characterize the role of SIRT2 during infection and identify all the genes at which it is recruited, we are performing ChIP-seq analysis. These studies are expected to bring new insights into the function and regulation of SIRT2 by characterizing this new phosphorylation site.
We are analyzing a Listeria protein secreted in the supernatant. From cells transfected with this protein, after crosslinking, we have isolated RNA and found the protein in the RNA fraction. In addition, the protein binds several splicing factors in RNA dependent manner. Furthemore, the protein localizes to the nucleus. In this project, we have isolated the protein from the supernatant and from bacterial extract after growth in BHI. We have extracted the RNA from the supernatant fraction containing the protein and from the bacterial extract containing the protein. We want to alalyze the RNA in these different fractions.
There exists a broad biodiversity inside the Listeria monocytogenes species, which can be summarized by the existence of evolutionary lineages and more than 100 clonal complexes (CCs or clones) based
Listeriolysin S (LLS) is a bacteriocin from Listeria monocytogenes that targets other Gram-positive bacteria, including Listeria monocytogenes itself. In order to understand the mechanism of action of