In the past Javier Pizarro-Cerdá has collaborated on articles with Stéphanie Seveau and Christian Demeure. One of their most recent publications is Scientific LifeSpecial Issue: 25 Years of Trends in Cell BiologyCell Biology and Microbiology: A Continuous Cross-Feeding. Which was published in journal Trends in Cell Biology.

More information about Javier Pizarro-Cerdá research including statistics on their citations can be found on their Copernicus Academic profile page.

Javier Pizarro-Cerdá's Articles: (7)

Scientific LifeSpecial Issue: 25 Years of Trends in Cell BiologyCell Biology and Microbiology: A Continuous Cross-Feeding

Microbiology and cell biology both involve the study of cells, albeit at different levels of complexity and scale. Interactions between both fields during the past 25 years have led to major conceptual and technological advances that have reshaped the whole biology landscape and its biomedical applications.

OpinionThe Diverse Family of Arp2/3 Complexes

TrendsMass spectrometry analysis of proteins extracted from focal adhesions identified two Arp2/3 hybrid complexes: the first is composed of Arp2, Arp3, ARPC2 and ARPC3 together with vinculin; the second is composed of Arp2, Arp3, ARPC2 and vinculin together with α-actinin.Functional studies of Arp2/3 complex subunits during Listeria monocytogenes cell invasion and actin-based motility suggest that diverse complexes participate at each infection stage. The subunit ARPC1B is predominantly required for cellular entry while the subunit ARPC1A is predominantly required for intracellular actin polymerization. Moreover, the subunit ARPC5 is dispensable for both processes.Arp2/3 complexes containing the subunits ARPC1B and ARPC5B are more efficient at promoting actin assembly by vaccinia virus than complexes containing ARPC1A and ARPC5A subunits.Post-translational modifications of different subunits affect the efficiency of Arp2/3 complex activity. Phosphorylation of Arp2 and ARPC1B enhances actin nucleation, while phosphorylation of Arp3 attenuates it.

ReviewManipulation of host membranes by the bacterial pathogens Listeria, Francisella, Shigella and Yersinia

AbstractBacterial pathogens display an impressive arsenal of molecular mechanisms that allow survival in diverse host niches. Subversion of plasma membrane and cytoskeletal functions are common themes associated to infection by both extracellular and intracellular pathogens. Moreover, intracellular pathogens modify the structure/stability of their membrane-bound compartments and escape degradation from phagocytic or autophagic pathways. Here, we review the manipulation of host membranes by Listeria monocytogenes, Francisella tularensis, Shigella flexneri and Yersinia spp. These four bacterial model pathogens exemplify generalized strategies as well as specific features observed during bacterial infection processes.

ForumMolecular mechanisms exploited by Listeria monocytogenes during host cell invasion

AbstractThe facultative intracellular bacterial pathogen Listeria monocytogenes has evolved multiple strategies to invade a large panel of mammalian cells. Host cell invasion is critical for several stages of listeriosis pathology such as the initial crossing of the host intestinal barrier and the successive colonization of diverse target organs including the placenta. In this review, we address the main molecular mechanisms known to be used by L. monocytogenes during invasion of nonphagocytic cells and host tissues.

Yersinia pestis and plague: an updated view on evolution, virulence determinants, immune subversion, vaccination and diagnostics

AbstractPlague is a vector-borne disease caused by Yersinia pestis. Transmitted by fleas from rodent reservoirs, Y. pestis emerged less than 6000 years ago from an enteric bacterial ancestor through events of gene gain and genome reduction. It is a highly remarkable model for the understanding of pathogenic bacteria evolution, and a major concern for public health as highlighted by recent human outbreaks. A complex set of virulence determinants, including the Yersinia outer membrane proteins (Yops), the broad range protease Pla, pathogen-associated molecular patterns (PAMPs) and iron capture systems play critical roles in the molecular strategies that Y. pestis employs to subvert the human immune system, allowing unrestricted bacterial replication in lymph nodes (bubonic plague) and in lungs (pneumonic plague). Some of these immunogenic proteins as well as the capsular antigen F1 are exploited for diagnostic purposes, which are critical in the context of the rapid onset of death in the absence of antibiotic treatment (less than a week for bubonic plague and less than 48 h for pneumonic plague). In here, we review recent research advances on Y. pestis evolution, virulence factors function, bacterial strategies to subvert mammalian innate immune responses, vaccination and problems associated to pneumonic plague diagnosis.

Microbiology / MicrobiologieExploitation of host cell cytoskeleton and signalling during Listeria monocytogenes entry into mammalian cellsExploitation du cytosquelette et de la machinerie de signalisation de la cellule hôte pendant l'entrée de Listeria monocytogenes

AbstractDeciphering how Listeria monocytogenes exploits the host cell machinery to invade mammalian cells during infection is a key issue for the understanding how this food-borne pathogen causes a pleiotropic disease ranging from gastro-enteritis to meningitis and abortions. Using multidisciplinary approaches, essentially combining bacterial genetics and cell biology, we have identified two bacterial proteins critical for entry into target cells, InlA and InlB. Their cellular ligands have been also identified: InlA interacts with the adhesion molecule E-cadherin, while InlB interacts with the receptor for the globular head of the complement factor C1q (gC1q-R), with the hepatocyte growth factor receptor (c-Met) and with glycosaminoglycans (including heparan sulphate). The dynamic interaction between these cellular receptors and the actin cytoskeleton is currently under investigation. Several intracellular molecules have been recognized as key effectors for Listeria entry into target cells, including catenins (implicated in the connection of E-cadherin to actin) and the actin depolymerising factor/cofilin (involved in the rearrangement of the cytoskeleton in the InlB-dependent internalisation pathway). At the organism level, species specificity has been discovered concerning the interaction between InlA and E-cadherin, leading to the generation of transgenic mice expressing the human E-cadherin, in which the critical role of InlA in the crossing of the intestinal barrier has been clearly determined. Listeria appears as an instrumental model for addressing critical questions concerning both the complex process of bacterial pathogenesis and also fundamental molecular processes, such as phagocytosis. To cite this article: J. Pizarro-Cerdá et al., C. R. Biologies 327 (2004).

Brucella abortus invasion and survival within professional and nonprofessional phagocytes

Publisher SummaryAs in the case of other cell associated bacteria of the alpha-2 subdivision, the fine adjustments between brucellae and their preferred host seem to be the result of a prolonged and intimate association between both parties. It is likely, as proposed in this work, that the ability of brucellae to adsorb, invade, survive, and reproduce inside phagocytic and nonphagocytic cells is multifactoriai, involving several components. At least in the case of Brucella species, this need to overcome the concept that virulence is related to a single or a few conditions but rather to a complexity of factors that efficiently interact for parasitism. The very existence of this complexity for adaptation to intracellular life is in itself one of the most significant pieces of evidence of the process that is called “evolution.”

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