Pedro Escoll

Centre National de la Recherche Scientifique

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Carmen Buchrieser

Centre National de la Recherche Scientifique

Mariatou Dramé

Université Paris Cité

Monica Rolando

Université Paris Cité

Christophe Rusniok

Institut Pasteur

Silke Schmidt

Institut Pasteur

Tobias Sahr

Institut Pasteur

Lucien Platon

Université de Strasbourg

Laura Gómez-Valero

Institut Pasteur

Sonia Mondino

Institut Pasteur

Eduardo López‐Collazo

Hospital Universitario La Paz

Cooperative Institutions

Institut Pasteur

Centre National de la Recherche Scientifique

Université Paris Cité

Inserm

Sorbonne Université

Consejo Superior de Investigaciones Científicas

Hospital Universitario La Paz

Universidade de São Paulo

Sorbonne Paris Cité

Clinics Hospital of Ribeirão Preto

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Manipulation of Autophagy by Bacterial Pathogens Impacts Host Immunity

Current Issues in Molecular Biology (2017)

T. Kunz Flávia Viana Carmen Buchrieser Pedro Escoll

Autophagy is a highly conserved catabolic process, degrading unnecessary or damaged components in the eukaryotic cell to maintain cellular homeostasis, but it is also an intrinsic cellular defence mechanism to remove invading pathogens. A crosstalk between autophagy and innate or adaptive immune responses has been recently reported, whereby autophagy influences both, innate and adaptive immunity like the production and secretion of pro-inflammatory cytokines or MHC class II antigen presentation to T cells. Pathogenic bacteria have evolved diverse strategies to manipulate autophagy, mechanisms that also impact host immune responses at different levels. Here we discuss the influence of autophagy on self-autonomous, innate and adaptive immunity and then focus on how bacterial mechanisms that shape autophagy may impact the host immune system.

Crosstalk

10.21775/cimb.025.081

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Citations (5)

Somatic tetraploidy in specific chick retinal ganglion cells induced by nerve growth factor

Proceedings of the National Academy of Sciences (2009)

Sandra M. Morillo Pedro Escoll Antonio de la Hera José M. Frade

A subset of neurons in the normal vertebrate nervous system contains double the normal amount of DNA in their nuclei. These neurons are all thought to derive from aberrant mitoses in neuronal precursor cells. Here we show that endogenous NGF induces DNA replication in a subpopulation of differentiating chick retinal ganglion cells that express both the neurotrophin receptor p75 and the E2F1 transcription factor, but that lack the retinoblastoma protein. Many of these neurons avoid G2/M transition and remain alive in the retina as tetraploid cells with large cell somas and extensive dendritic trees, and most of them express beta2 nicotinic acetylcholine receptor subunits, a specific marker of retinal ganglion cells innervating lamina F in the stratum-griseum-et-fibrosum-superficiale of the tectal cortex. Tetraploid neurons were also observed in the adult mouse retina. Thus, a developmental program leading to somatic tetraploidy in specific retinal neurons exists in vertebrates. This program might occur in other vertebrate neurons during normal or pathological situations.

10.1073/pnas.0906121107

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Citations (55)

Modulation of Host Autophagy during Bacterial Infection: Sabotaging Host Munitions for Pathogen Nutrition

Frontiers in Immunology (2016)

Pedro Escoll Monica Rolando Carmen Buchrieser

OPINION article Front. Immunol., 03 March 2016Sec. Microbial Immunology Volume 7 - 2016 | https://doi.org/10.3389/fimmu.2016.00081

10.3389/fimmu.2016.00081

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Citations (49)

Roles of Mitochondrial Respiratory Complexes during Infection

Immunometabolism (2019)

Pedro Escoll Lucien Platon Carmen Buchrieser

Abstract Beyond oxidative phosphorylation (OXPHOS), mitochondria have also immune functions against infection, such as the regulation of cytokine production, the generation of metabolites with antimicrobial proprieties and the regulation of inflammasome-dependent cell death, which seem in turn to be regulated by the metabolic status of the organelle. Although OXPHOS is one of the main metabolic programs altered during infection, the mechanisms by which pathogens impact the mitochondrial electron transport chain (ETC) complexes to alter OXPHOS are not well understood. Similarly, how changes on ETC components affect infection is only starting to be characterized. Herein we summarize and discuss the existing data about the regulation of ETC complexes and super-complexes during infection, in order to shed some light on the mechanisms underlying the regulation of the mitochondrial OXPHOS machinery when intracellular pathogens infect eukaryotic host cells.

Organelle

Mitochondrial respiratory chain

10.20900/immunometab20190011

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Citations (19)

Metabolic reprogramming: an innate cellular defence mechanism against intracellular bacteria?

Current Opinion in Immunology (2019)

Pedro Escoll Carmen Buchrieser

Intracellular parasite

Reprogramming

Metabolic pathway

10.1016/j.coi.2019.05.009

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Citations (45)

Legionella pneumophila restrains autophagy by modulating the host's sphingolipid metabolism

Autophagy (2016)

Monica Rolando Pedro Escoll Carmen Buchrieser

Sphingolipids are bioactive molecules playing a key role as membrane components, but they are also central regulators of many intracellular processes including macroautophagy/autophagy. In particular, sphingosine-1-phosphate (S1P) is a critical mediator that controls the balance between sphingolipid-induced autophagy and cell death. S1P levels are adjusted via S1P synthesis, dephosphorylation or degradation, catalyzed by SGPL1 (sphingosine-1-phosphate lyase 1). Intracellular pathogens are able to modulate many different host cell pathways to allow their replication. We have found that infection of eukaryotic cells with the human pathogen Legionella pneumophila triggers a change in the host cell sphingolipid metabolism and specifically affects the levels of sphingosine. Indeed, L. pneumophila secretes a protein highly homologous to eukaryotic SGPL1 (named LpSPL). We solved the crystal structure of LpSPL and showed that it encodes lyase activity, targets the host's sphingolipid metabolism, and plays a role in starvation-induced autophagy during L. pneumophila infection to promote intracellular survival.

Sphingolipid

Sphingosine Kinase

Intracellular parasite

10.1080/15548627.2016.1166325

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Citations (30)

Visualizing mitochondrial electron transport chain complexes and super-complexes during infection of human macrophages with Legionella pneumophila

Methods in cell biology (2024)

Mariatou Dramé Daniel Schator Carmen Buchrieser Pedro Escoll

Legionella

10.1016/bs.mcb.2024.01.003

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MAMs are attractive targets for bacterial repurposing of the host cell

BioEssays (2016)

Pedro Escoll Monica Rolando Carmen Buchrieser

Pathogenic bacteria frequently target the endoplasmic reticulum (ER) and mitochondria in order to exploit host functions. ER‐mitochondria inter‐organelle communication is topologically sub‐compartmentalized at mitochondria‐associated ER membranes (MAMs). MAMs are specific membranous microdomains with unique regulatory functions such as lipid synthesis and trafficking, calcium homeostasis, mitochondrial morphology, inflammasome activation, autophagosome formation, and apoptosis. These important cellular processes are all modulated by pathogens to subvert host functions and promote infection, thus it is tempting to assume that pathogenic bacteria target MAMs to subvert these different pathways in their hosts. First lines of evidence that support this hypothesis come from Legionella pneumophila . This intracellular bacterium secretes an effector that exhibits sphingosine‐1 phosphate lyase activity ( Lp Spl) that seems to target MAMs to modulate the autophagy response to infection. Here we thus propose the concept that MAMs could be targeted by pathogenic bacteria to undermine key host cellular processes.

Pathogenic bacteria

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Endomembrane system

10.1002/bies.201600171

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Citations (16)

Ordering human CD34⁺CD10⁻CD19⁺pre/pro-B-cell and CD19⁻common lymphoid progenitor stages in two pro-B-cell development pathways

Proceedings of the National Academy of Sciences (2010)

Eva Sanz Norman Muñoz-A.Jorge Monserrat Ana Maria Van Den Rym Pedro Escoll

Studies here respond to two long-standing questions: Are human "pre/pro-B" CD34(+)CD10(-)CD19(+) and "common lymphoid progenitor (CLP)/early-B" CD34(+)CD10(+)CD19(-) alternate precursors to "pro-B" CD34(+)CD19(+)CD10(+) cells, and do the pro-B cells that arise from these progenitors belong to the same or distinct B-cell development pathways? Using flow cytometry, gene expression profiling, and Ig V(H)-D-J(H) sequencing, we monitor the initial 10 generations of development of sorted cord blood CD34(high)Lineage(-) pluripotential progenitors growing in bone marrow S17 stroma cocultures. We show that (i) multipotent progenitors (CD34(+)CD45RA(+)CD10(-)CD19(-)) directly generate an initial wave of Pax5(+)TdT(-) "unilineage" pre/pro-B cells and a later wave of "multilineage" CLP/early-B cells and (ii) the cells generated in these successive stages act as precursors for distinct pro-B cells through two independent layered pathways. Studies by others have tracked the origin of B-lineage leukemias in elderly mice to the mouse B-1a pre/pro-B lineage, which lacks the TdT activity that diversifies the V(H)-D-J(H) Ig heavy chain joints found in the early-B or B-2 lineage. Here, we show a similar divergence in human B-cell development pathways between the Pax5(+)TdT(-) pre/pro-B differentiation pathway that gives rise to infant B-lineage leukemias and the early-B pathway.

Lymphopoiesis

PAX5

10.1073/pnas.0907942107

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Citations (53)

Targeting of host organelles by pathogenic bacteria: a sophisticated subversion strategy

Nature Reviews Microbiology (2015)

Pedro Escoll Sonia Mondino Monica Rolando Carmen Buchrieser

Organelle

10.1038/nrmicro.2015.1

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Citations (141)