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    Team: Cell signaling in bacterial infections.


    Team leader

    Bacterial infections represent a rising threat on human health. They result from complex molecular interactions between a large number of microbial components and host factors, and therefore, need to be addressed on a global scale. Using the enteroinvasive bacterium Shigella flexneri as main model of infection, we combine systems biology methods and mechanistic approaches to characterize the host molecular pathways involved in several key aspects of bacterial infections including invasion of epithelial cells, host cell survival and inflammation.


    The emergence of multi-drug-resistance mechanisms among major pathogenic bacteria represents a rising threat on human health. The lack of new therapeutic options requires an urgent effort of the scientific community to identify new microbial targets and envision alternative strategies. A promising approach consists of targeting the host instead of the pathogen. Indeed, it became clear over the last years, that pathogens subvert key cellular factors and responses in order to infect their host. Blocking the expressing of these factors or interfering with their activities may prevent colonization and have a positive impact on the infection outcome. Since infections result from countless molecular interactions between microbial components and host factors, identifying key cellular targets requires mapping these interactions on a global scale.

    Using the enteroinvasive bacterium Shigella flexneri as main model, we apply systems biology methods including large scale RNAi screens and phosphoproteomics to identify and characterize the cellular pathways that are required for bacterial invasion of epithelial cells, survival of infected cells and inflammation, three central aspects of S. flexneri pathogenesis.

    Main publications

    Schmutz C, Ahrne EL, Kasper CA, Tschon T, Sorg I, Dreier RF, Schmidt A, Arrieumerlou C. Systems-level overview of host protein phosphorylation during Shigella flexneri infection revealed by phosphoproteomics. Mol Cell Proteomics. 2013 Oct; 12(10):2952-68.

    Kasper, C. A., Sorg, I., Schmutz, C., Tschon, T., Wischnewski, H., Kim, M. L. and Arrieumerlou, C. (2010). Cell-Cell Propagation of NF-kappaB Transcription Factor and MAP Kinase Activation Amplifies Innate Immunity against Bacterial Infection. Immunity, 33(5), 804–816.

    Reiterer, V., Grossniklaus, L., Tschon, T., Kasper, C. A., Sorg, I. and Arrieumerlou C. Shigella flexneri type III secreted effector OspF reveals new crosstalks of proinflammatory signaling pathways during bacterial infection. Cell Signal. 2011 Jul; 23(7):1188-96.

    Kim, M. L., Jeong, H. G., Kasper, C. A. and Arrieumerlou, C. (2010). IKKalpha Contributes to Canonical NF-kappaB Activation Downstream of Nod1-Mediated Peptidoglycan Recognition. PLoS One, 5(10), e15371.

    Malone, J. G., Jaeger, T., Spangler, C., Ritz, D., Spang, A., Arrieumerlou, C., Kaever, V., Landmann, R. and Jenal, U. (2010). YfiBNR Mediates Cyclic di-GMP Dependent Small Colony Variant Formation and Persistence in Pseudomonas aeruginosa. PLoS Pathog, 6(3), e1000804

    Team's news

    • Recruitment to the Cochin Institute through the 2013 international recruitment campaign.
    • Move from the Biozentrum (University of Basel) to Paris. Opening of the lab at the Cochin Institute on January 1st 2014 (Méchain building, 3rd floor, room 313).
    • Milica Milivojevic, first master student in the lab in Paris, obtains a PhD fellowship from the Bio Sorbonne Paris Cité (BioSPC) PhD program.
    • Anne-Sophie Dangeard, engineer, joins the group (January 2015).