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Search Results: 1 - 10 of 1851 matches for " Serge Mostowy "
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Multiple Roles of the Cytoskeleton in Bacterial Autophagy
Serge Mostowy
PLOS Pathogens , 2014, DOI: doi/10.1371/journal.ppat.1004409
Abstract:
Septins Regulate Bacterial Entry into Host Cells
Serge Mostowy, To Nam Tham, Anne Danckaert, Stéphanie Guadagnini, Stéphanie Boisson-Dupuis, Javier Pizarro-Cerdá, Pascale Cossart
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0004196
Abstract: Background Septins are conserved GTPases that form filaments and are required in many organisms for several processes including cytokinesis. We previously identified SEPT9 associated with phagosomes containing latex beads coated with the Listeria surface protein InlB. Methodology/Principal Findings Here, we investigated septin function during entry of invasive bacteria in non-phagocytic mammalian cells. We found that SEPT9, and its interacting partners SEPT2 and SEPT11, are recruited as collars next to actin at the site of entry of Listeria and Shigella. SEPT2-depletion by siRNA decreased bacterial invasion, suggesting that septins have roles during particle entry. Incubating cells with InlB-coated beads confirmed an essential role for SEPT2. Moreover, SEPT2-depletion impaired InlB-mediated stimulation of Met-dependent signaling as shown by FRET. Conclusions/Significance Together these findings highlight novel roles for SEPT2, and distinguish the roles of septin and actin in bacterial entry.
PhoP: A Missing Piece in the Intricate Puzzle of Mycobacterium tuberculosis Virulence
Jesús Gonzalo-Asensio, Serge Mostowy, Jose Harders-Westerveen, Kris Huygen, Rogelio Hernández-Pando, Jelle Thole, Marcel Behr, Brigitte Gicquel, Carlos Martín
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0003496
Abstract: Inactivation of the transcriptional regulator PhoP results in Mycobacterium tuberculosis attenuation. Preclinical testing has shown that attenuated M. tuberculosis phoP mutants hold promise as safe and effective live vaccine candidates. We focused this study to decipher the virulence networks regulated by PhoP. A combined transcriptomic and proteomic analysis revealed that PhoP controls a variety of functions including: hypoxia response through DosR crosstalking, respiratory metabolism, secretion of the major T-cell antigen ESAT-6, stress response, synthesis of pathogenic lipids and the M. tuberculosis persistence through transcriptional regulation of the enzyme isocitrate lyase. We also demonstrate that the M. tuberculosis phoP mutant SO2 exhibits an antigenic capacity similar to that of the BCG vaccine. Finally, we provide evidence that the SO2 mutant persists better in mouse organs than BCG. Altogether, these findings indicate that PhoP orchestrates a variety of functions implicated in M. tuberculosis virulence and persistence, making phoP mutants promising vaccine candidates.
Recruitment of the Major Vault Protein by InlK: A Listeria monocytogenes Strategy to Avoid Autophagy
Laurent Dortet,Serge Mostowy,Ascel Samba Louaka,Edith Gouin,Marie-Anne Nahori,Erik A.C. Wiemer,Olivier Dussurget,Pascale Cossart
PLOS Pathogens , 2011, DOI: 10.1371/journal.ppat.1002168
Abstract: L. monocytogenes is a facultative intracellular bacterium responsible for listeriosis. It is able to invade, survive and replicate in phagocytic and non-phagocytic cells. The infectious process at the cellular level has been extensively studied and many virulence factors have been identified. Yet, the role of InlK, a member of the internalin family specific to L. monocytogenes, remains unknown. Here, we first show using deletion analysis and in vivo infection, that InlK is a bona fide virulence factor, poorly expressed in vitro and well expressed in vivo, and that it is anchored to the bacterial surface by sortase A. We then demonstrate by a yeast two hybrid screen using InlK as a bait, validated by pulldown experiments and immunofluorescence analysis that intracytosolic bacteria via an interaction with the protein InlK interact with the Major Vault Protein (MVP), the main component of cytoplasmic ribonucleoproteic particules named vaults. Although vaults have been implicated in several cellular processes, their role has remained elusive. Our analysis demonstrates that MVP recruitment disguises intracytosolic bacteria from autophagic recognition, leading to an increased survival rate of InlK over-expressing bacteria compared to InlK? bacteria. Together these results reveal that MVP is hijacked by L. monocytogenes in order to counteract the autophagy process, a finding that could have major implications in deciphering the cellular role of vault particles.
The Zebrafish as a New Model for the In Vivo Study of Shigella flexneri Interaction with Phagocytes and Bacterial Autophagy
Serge Mostowy ,Laurent Boucontet,Maria J. Mazon Moya,Andrea Sirianni,Pierre Boudinot,Michael Hollinshead,Pascale Cossart,Philippe Herbomel,Jean-Pierre Levraud,Emma Colucci-Guyon
PLOS Pathogens , 2013, DOI: 10.1371/journal.ppat.1003588
Abstract: Autophagy, an ancient and highly conserved intracellular degradation process, is viewed as a critical component of innate immunity because of its ability to deliver cytosolic bacteria to the lysosome. However, the role of bacterial autophagy in vivo remains poorly understood. The zebrafish (Danio rerio) has emerged as a vertebrate model for the study of infections because it is optically accessible at the larval stages when the innate immune system is already functional. Here, we have characterized the susceptibility of zebrafish larvae to Shigella flexneri, a paradigm for bacterial autophagy, and have used this model to study Shigella-phagocyte interactions in vivo. Depending on the dose, S. flexneri injected in zebrafish larvae were either cleared in a few days or resulted in a progressive and ultimately fatal infection. Using high resolution live imaging, we found that S. flexneri were rapidly engulfed by macrophages and neutrophils; moreover we discovered a scavenger role for neutrophils in eliminating infected dead macrophages and non-immune cell types that failed to control Shigella infection. We observed that intracellular S. flexneri could escape to the cytosol, induce septin caging and be targeted to autophagy in vivo. Depletion of p62 (sequestosome 1 or SQSTM1), an adaptor protein critical for bacterial autophagy in vitro, significantly increased bacterial burden and host susceptibility to infection. These results show the zebrafish larva as a new model for the study of S. flexneri interaction with phagocytes, and the manipulation of autophagy for anti-bacterial therapy in vivo.
Toward an integrative model for alcohol use and dependence  [PDF]
Serge Combaluzier
Open Journal of Psychiatry (OJPsych) , 2012, DOI: 10.4236/ojpsych.2012.24044
Abstract: Background: If the alcohol use and dependence disorders are differentiated by the pharmaco-dependence, they share complex relationships with other clinical disorders and personality disorders. The purpose of this paper is to produce a model that reflects its relations both among users than among addicts. Method: Data from questionnaires measuring key variables selected for this study have been collected from people with alcohol misuse (n = 83) and alcohol-dependent (n = 81) in rehab. A model of drug dependence has been produced from these data that gives complete satisfaction to the criteria of SEM. Discussion: This model reflects the shift from abuse to a dependent consumption by the presence of feedbacks involving pharmaco-dependence, disturbance of the alcohol consumption by psychological distress and depressive traits. To further guarantee its validity, however it should be tested by collecting data from other surveys.
Non-genetic inheritance and the patterns of antagonistic coevolution
Rafal Mostowy, Jan Engelst?dter, Marcel Salathé
BMC Evolutionary Biology , 2012, DOI: 10.1186/1471-2148-12-93
Abstract: Here, we show that another factor – non-genetic inheritance, mediated for example by epigenetic mechanisms – can completely eliminate oscillations in the presence of such negative frequency dependence, even if only a small fraction of offspring are affected. We analytically derive the threshold value of this fraction at which the dynamics change from oscillatory to stable, and investigate how selection, mutation and generation times differences between the two species affect the threshold value. These results strongly suggest that the lack of phenotype frequency oscillations should not be attributed to the lack of strong interactions between antagonistic species.Given increasing evidence of non-genetic effects on the outcomes of antagonistic species interactions, we suggest that these effects should be incorporated into ecological and evolutionary models of interacting species.
Evolution of Stress Response in the Face of Unreliable Environmental Signals
Markus Arnoldini ,Rafal Mostowy ,Sebastian Bonhoeffer,Martin Ackermann
PLOS Computational Biology , 2012, DOI: 10.1371/journal.pcbi.1002627
Abstract: Most organisms live in ever-changing environments, and have to cope with a range of different conditions. Often, the set of biological traits that are needed to grow, reproduce, and survive varies between conditions. As a consequence, organisms have evolved sensory systems to detect environmental signals, and to modify the expression of biological traits in response. However, there are limits to the ability of such plastic responses to cope with changing environments. Sometimes, environmental shifts might occur suddenly, and without preceding signals, so that organisms might not have time to react. Other times, signals might be unreliable, causing organisms to prepare themselves for changes that then do not occur. Here, we focus on such unreliable signals that indicate the onset of adverse conditions. We use analytical and individual-based models to investigate the evolution of simple rules that organisms use to decide whether or not to switch to a protective state. We find evolutionary transitions towards organisms that use a combination of random switching and switching in response to the signal. We also observe that, in spatially heterogeneous environments, selection on the switching strategy depends on the composition of the population, and on population size. These results are in line with recent experiments that showed that many unicellular organisms can attain different phenotypic states in a probabilistic manner, and lead to testable predictions about how this could help organisms cope with unreliable signals.
The Role of Recombination for the Coevolutionary Dynamics of HIV and the Immune Response
Rafal Mostowy,Roger D. Kouyos,David Fouchet,Sebastian Bonhoeffer
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0016052
Abstract: The evolutionary implications of recombination in HIV remain not fully understood. A plausible effect could be an enhancement of immune escape from cytotoxic T lymphocytes (CTLs). In order to test this hypothesis, we constructed a population dynamic model of immune escape in HIV and examined the viral-immune dynamics with and without recombination. Our model shows that recombination (i) increases the genetic diversity of the viral population, (ii) accelerates the emergence of escape mutations with and without compensatory mutations, and (iii) accelerates the acquisition of immune escape mutations in the early stage of viral infection. We see a particularly strong impact of recombination in systems with broad, non-immunodominant CTL responses. Overall, our study argues for the importance of recombination in HIV in allowing the virus to adapt to changing selective pressures as imposed by the immune system and shows that the effect of recombination depends on the immunodominance pattern of effector T cell responses.
Health 3.0—The patient-clinician “arabic spring” in healthcare  [PDF]
Serge Gagnon, Laurent Chartier
Health (Health) , 2012, DOI: 10.4236/health.2012.42008
Abstract: A growing number of citizen-patients and clinicians use Communication and Self-Managed Health Technologies (CSMHT) in their relationship. Doing so, they shift from the current paradigm of dependency to a co-responsibility paradigm in healthcare. Facing the runaway utilization of health services, we need to think “outside the box” to unblock the system. A Health 3.0 development model of governance that position patients as primary members of the clinicians’ team is presented to map this institutional transformation. At the practical level, an MD 3.0 relational model and a Citizen-Patient 3.0 behavioral profile are presented.
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