Vendredi
03/11/2017
11h

Salle des Thèses Chantal Rabourdin-Combe

Pr. Nicolas DUPIN -  Hôpital Cochin, APHP, Paris           

contact marc.vocanson@inserm.fr

Propionibacterium acnes_ (P. acnes) est une bactérie majeure associée à la peau qui a longtemps été considérée comme une bactérie commensale, jusqu' à ce que plusieurs études révèlent  qu'elle est un pathogène opportuniste impliqué dans plusieurs infections invasives. P. acnes induit une réponse inflammatoire importante via l’activation de la voie TLR2 et du recepteur CD36 associé à la NADPH oxidase (NOX1) dans les cellules de l’immunité innée et les kératinocytes conduisant à la production de cytokines et chemokines proinflammatoires et un « burst » oxidatif très important. A ce jour, le rôle de P. acnes et les mécanismes moléculaires mis en jeux lors de l’apparition de ces réactions inflammatoires restent mal connus. Notre travail s’inscrit dans la caractérisation des mécanismes moléculaires impliqués dans la relation de P. acnes avec son hôte. Plus particulièrement, nous étudions les protéines de surfaces de P. acnes qui sont impliquées dans le processus inflammatoire et dans l’interaction avec les protéines de la matrice extracellulaire de l’hôte.

Lundi
06/11/2017
11h

Salle de conférence IBCP

Urs JENAL - Biozentrum, University of Basel, Switzerland

invited by C. Grangeasse

Vendredi
10/11/2017
11h

Salle Condorcet*

Irina SOLOVEI - LMU Munich

 Hôte : Geneviève Fourel

* Salle CONDORCET - ex Conférence 1 Place de l’Ecole – Site Monod ENS

Lundi
13/11/2017
11h

Salle des Thèses Chantal Rabourdin-Combe

Pekka KATAJISTO - Associate professor at Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Finland and Director of the Centre of Excellence in Stem Cell Metabolism at the Academy of Finland

Hôte : Kiran Padmanabhan

Stem cells can divide asymmetrically to generate one daughter cell that will differentiate, and another that retains stem cell traits. Such asymmetry opens the possibility that stem cells segregate their sub-cellular components selectively during cell division, and thereby reduce damage accumulation in the stem cell lineage. We used chronologic age of sub-cellular components, such as organelles, as a proxy for damage they may have sustained, and discovered that stem-like cells of the mammary epithelium apportion their mitochondria age-selectively and asymmetrically between daughter cells (Katajisto, Science, 2015). More specifically, old mitochondria are segregated away from the stem cell lineage into the differentiating daughter cells. I will describe our current work on how old and young mitochondria differ, and the functional relevance of age-selective organelle segregation by stem cells.

Lundi
13/11/2017
14h

Salle des Thèses Chantal Rabourdin-Combe

Thomas SURREY - The Francis Crick institut, UK

Lundi
13/11/2017
11h

Salle de conférence IBCP

Ben WISEMAN - Stockholm university, Sweden

invited by P. Falson

Lundi
20/11/2017
11h

Salle de conférence IBCP

Lutz SCHMITT- Institute of Biochemistry, Heinrich Heine University Düsseldorf, Germany                        

invited by J.M. Jault

Gram-negative bacteria have evolved at least six dedicated secretion systems to translocate proteins of diverse function into the extracellular media or directly into the host cell. Among these, the most “simple” system is the Type 1 secretion system (T1SS) as it is composed of only three components, an ABC transporter and a membrane fusion protein (MFP), both residing in the inner membrane, and an outer membrane protein (OMP). Common to all substrates of T1SS is a C-terminal secretion sequence that is not cleaved during or after transport. Furthermore, one prominent family of substrates contain Asp- and Gly-rich nonapeptide sequences, the so-called GG repeats. These GG repeats form the RTX (repeat in toxins) domain and are responsible for binding of Ca2+ in the extracellular space, which triggers folding of the entire substrate.
One of the best-studied T1SS is the hemolysin (Hly) A secretion system. Here, HlyB (ABC transporter), HlyD (MFP) and TolC (OMP) form the translocation machinery that secrets unfolded HlyA, a 110 kDa toxin that lysis many human cells and is a central virulence factor during urinary tract infection. However, the translocation machinery is apparently only transiently assembled in the presence of the substrate likely through interactions of the substrates with HlyB and / or HlyD. This interaction results in the recruitment of TolC and formation of the channel-tunnel, through which HlyA is secreted in one step from the cytosol into the extracellular media at the dispense of ATP hydrolysis by the ABC transporter HlyB.
Here, I will summarize our recent results with respect to a quantitative understanding of how this nanomachinery achieves the translocation of a substrate of approximately 1000 amino acids across two biological membranes in one step.

Mardi
22/11/2017
11h

Salle des Thèses Chantal Rabourdin-Combe

 keynote seminar

Prof. David W. HOLDEN - MRC Centre for Molecular Bacteriology and Infection, Imperial College London

Contact : suzana.salcedo@ibcp.fr

Salmonella enterica can cause persistent infections such as typhoid fever. Following bacterial entry into host cells, the pathogen replicates in a membrane-bound compartment called the Salmonella-containing vacuole (SCV). Bacteria respond to nutritional deprivation and the acidic pH in the vacuole lumen by activating the expression of the SPI-2 type III secretion system (T3SS). After assembly of a T3SS-linked pore in the vacuole membrane, bacteria sense the near-neutral pH of the host cell cytoplasm. This triggers the translocation of bacterial virulence proteins (effectors) into the host cell.
Approximately 30 different effectors are translocated by the SPI-2 T3SS. These have been implicated in several physiological activities, including the control of SCV positioning within the host cell, maintenance of vacuole membrane integrity, bacterial replication, interference with lysosome function and innate immune signaling. I will discuss our recent progress on an effector that suppresses the development of adaptive immunity, which is likely to contribute to the ability of Salmonella to persist in host tissues.
For more information here is a description of his work: http://www.imperial.ac.uk/people/d.holden

Jeudi
23/11/2017
13h30

Salle des Thèses Chantal Rabourdin-Combe

Jonathan LOPEZ - Plateforme BIOGENET Lyon-Sud

contact: denise.aubert@ens-lyon.fr

The translational research platform of Hospices Civils de Lyon, located at Lyon Sud University Hospital, offers you access to cutting-edge technologies in biopathology and molecular biology within a partnership with academics or industrials. This includes the 3D biology approach developped by NanoString that allows you to simultaneously analyse nucleic and protein targets on a single biological sample in a highly multipliable fashion. What if we could do this multi-genomic analysis directly on a tissu slide with a single-celle resolution? That is exactly what the Digital Space Profiling approach offers.

Vendredi
24/11/2017
14h30

Amphi Pasteur - Tour Inserm CERVI *

Forum d’infectiologie

Pr. Alain FILLOUX - Imperial College London, MRC Centre for Molecular Bacteriology and Infection, London – UK

Contact : karen.moreau@univ-lyon1.fr

Alain Filloux a obtenu son doctorat en 1988 à l'Université d'Aix-Marseille (France). De 1988 à 1993, il a séjourné à l'Université d'Utrecht (Pays-Bas), d'abord en tant que post-doc, puis comme professeur adjoint. En 1994, il est recruté au CNRS de Marseille (France) où il est nommé directeur d'une unité de recherche en 2003. En 2008, il est nommé professeur de microbiologie moléculaire à l'Imperial College London (Royaume-Uni) et il est directeur adjoint du Centre de biologie moléculaire et d'infection. En 2013, il est nommé rédacteur en chef pour FEMS Microbiology Reviews. Ses recherches portent principalement sur la pathogenèse bactérienne, les mécanismes moléculaires de la sécrétion de protéines, la formation de biofilms et la régulation de l'expression génique. Le modèle de système qu'il a utilisé est le pathogène bactérien Pseudomonas aeruginosa.

* Merci aux visiteurs de se munir d’une pièce d’identité valide (carte d’identité ou passeport – Permis de conduire non valable) pour accéder à l’amphithéâtre Pasteur.

Lundi
27/11/2017
11h

Salle de conférence IBCP

Sophie HÉLAINE - Imperial College, London               

invited by S. Salcedo            

Vendredi
01/12/2017
11h

Amphi Pasteur - Tour Inserm CERVI *

Forum d’infectiologie

Fernando MACIAN JUAN - Albert Einstein College of Medicine Dpt of Pathology and Institute for Aging Research Bronx – NY – USA

Contact : mathias.faure@inserm.fr

Fernando MACIAN JUAN has more than 20 years of experience in the study and characterization of the molecular mechanisms that regulate T cell activation and tolerance. His group has pioneered the identification and characterization of the signaling pathways, transcriptional complexes and molecular events that regulate the functional outcome following T cell receptor engagement in peripheral T cells. His studies have contributed to the identification of the transcriptional and signaling events that regulate T cell fate upon antigen encounter and determine T helper cell differentiation, activation and tolerance. In the last 10 years, his group has helped defined the roles and regulation of different forms of autophagy in T cell biology and has contributed to the establishment of autophagy as an essential cell process in the modulation of T helper cell responses.

* Merci aux visiteurs de se munir d’une pièce d’identité valide (carte d’identité ou passeport – Permis de conduire non valable) pour accéder à l’amphithéâtre Pasteur.