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  1. Article ; Online: Editorial: The Autophagy Pathway: Bacterial Pathogen Immunity and Evasion.

    Jagannath, Chinnaswamy / McBride, Jere W / Vergne, Isabelle

    Frontiers in immunology

    2021  Volume 12, Page(s) 768935

    MeSH term(s) Animals ; Autophagy/immunology ; Bacteria/immunology ; Bacterial Infections/immunology ; Bacterial Infections/microbiology ; Host-Pathogen Interactions/immunology ; Humans ; Immune Evasion/immunology ; Signal Transduction/immunology
    Language English
    Publishing date 2021-09-28
    Publishing country Switzerland
    Document type Editorial ; Introductory Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.768935
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Macrophage Autophagy and Bacterial Infections.

    Bah, Aïcha / Vergne, Isabelle

    Frontiers in immunology

    2017  Volume 8, Page(s) 1483

    Abstract: Autophagy is a well-conserved lysosomal degradation pathway that plays key roles in bacterial infections. One of the most studied is probably xenophagy, the selective capture and degradation of intracellular bacteria by lysosomes. However, the impact of ... ...

    Abstract Autophagy is a well-conserved lysosomal degradation pathway that plays key roles in bacterial infections. One of the most studied is probably xenophagy, the selective capture and degradation of intracellular bacteria by lysosomes. However, the impact of autophagy goes beyond xenophagy and involves intensive cross-talks with other host defense mechanisms. In addition, autophagy machinery can have non-canonical functions such as LC3-associated phagocytosis. In this review, we intend to summarize the current knowledge on the many functions of autophagy proteins in cell defenses with a focus on bacteria-macrophage interaction. We also present the strategies developed by pathogens to evade or to exploit this machinery in order to establish a successful infection. Finally, we discuss the opportunities and challenges of autophagy manipulation in improving therapeutics and vaccines against bacterial pathogens.
    Language English
    Publishing date 2017
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2017.01483
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Pharaoh's snakes of the teasel: New insights into Francis Darwin's observations.

    Vergne, Antoine / Giraud, Eric / Camuel, Alicia / Bardot, Corinne / Billard, Hermine / Bouquet, Clémentin / Corbara, Bruno / Gully, Djamel / Mathonat, Frédéric / Jeanthon, Christian / Mary, Isabelle / Caissard, Jean-Claude / Lehours, Anne-Catherine

    Ecology

    2023  Volume 104, Issue 5, Page(s) e4030

    MeSH term(s) Animals ; Dipsacaceae ; Biological Evolution ; Ants
    Language English
    Publishing date 2023-03-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2010140-5
    ISSN 1939-9170 ; 0012-9658
    ISSN (online) 1939-9170
    ISSN 0012-9658
    DOI 10.1002/ecy.4030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Where is the field of autophagy research heading?

    Abeliovich, Hagai / Debnath, Jayanta / Ding, Wen-Xing / Jackson, William T / Kim, Do-Hyung / Klionsky, Daniel J / Ktistakis, Nicholas / Margeta, Marta / Münz, Christian / Petersen, Morten / Sadoshima, Junichi / Vergne, Isabelle

    Autophagy

    2023  Volume 19, Issue 4, Page(s) 1049–1054

    Abstract: In this editors' corner, the section editors were asked to indicate where they see the autophagy field heading and to suggest what they consider to be key unanswered questions in their specialty area. ...

    Abstract In this editors' corner, the section editors were asked to indicate where they see the autophagy field heading and to suggest what they consider to be key unanswered questions in their specialty area.
    MeSH term(s) Autophagy ; Biomedical Research/trends
    Language English
    Publishing date 2023-01-23
    Publishing country United States
    Document type Editorial
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2023.2166301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The Lipid Virulence Factors of

    Bah, Aïcha / Sanicas, Merlin / Nigou, Jérôme / Guilhot, Christophe / Astarie-Dequeker, Catherine / Vergne, Isabelle

    Cells

    2020  Volume 9, Issue 3

    Abstract: Autophagy is an important innate immune defense mechanism that ... ...

    Abstract Autophagy is an important innate immune defense mechanism that controls
    MeSH term(s) Autophagy/immunology ; Bacterial Proteins/drug effects ; Bacterial Proteins/metabolism ; Humans ; Lipids/pharmacology ; Macrophages/drug effects ; Macrophages/metabolism ; Macrophages/microbiology ; Mycobacterium tuberculosis/drug effects ; Mycobacterium tuberculosis/metabolism ; Mycobacterium tuberculosis/pathogenicity ; Phagocytosis/drug effects ; Phagocytosis/immunology ; Phagosomes/metabolism ; Phagosomes/microbiology ; Virulence Factors/metabolism
    Chemical Substances Bacterial Proteins ; Lipids ; Virulence Factors ; phthiocerol dimycocerosate (63642-22-8)
    Language English
    Publishing date 2020-03-09
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells9030666
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Erratum to "BCGΔBCG1419c and BCG differ in induction of autophagy, c-di-GMP content, proteome, and progression of lung pathology in Mycobacterium tuberculosis HN878-infected male BALB/c mice" [Vaccine 41(26) (2023) 3824-3835].

    Aceves-Sánchez, Michel de Jesús / Barrios-Payán, Jorge Alberto / Segura-Cerda, Cristian Alfredo / Flores-Valdez, Mario Alberto / Mata-Espinosa, Dulce / Pedroza-Roldán, César / Yadav, Rahul / Saini, Deepak Kumar / de la Cruz, Miguel Angel / Ares, Miguel A / Bielefeldt-Ohmann, Helle / Baay-Guzmán, Guillermina / Vergne, Isabelle / Velázquez-Fernández, Jesús Bernardino / Barba León, Jeannette / Hernández-Pando, Rogelio

    Vaccine

    2024  Volume 42, Issue 7, Page(s) 1852–1853

    Language English
    Publishing date 2024-02-15
    Publishing country Netherlands
    Document type Published Erratum
    ZDB-ID 605674-x
    ISSN 1873-2518 ; 0264-410X
    ISSN (online) 1873-2518
    ISSN 0264-410X
    DOI 10.1016/j.vaccine.2024.02.030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: La phagocytose associée à LC3 (LAP) - Phagocytose ou autophagie ?

    Galais, Mathilde / Pradel, Baptiste / Vergne, Isabelle / Robert-Hebmann, Véronique / Espert, Lucile / Biard-Piechaczyk, Martine

    Medecine sciences : M/S

    2019  Volume 35, Issue 8-9, Page(s) 635–642

    Abstract: Phagocytosis and macroautophagy, named here autophagy, are two essential mechanisms of lysosomal degradation of diverse cargos into membrane structures. Both mechanisms are involved in immune regulation and cell survival. However, phagocytosis triggers ... ...

    Title translation LAP (LC3-associated phagocytosis): phagocytosis or autophagy?
    Abstract Phagocytosis and macroautophagy, named here autophagy, are two essential mechanisms of lysosomal degradation of diverse cargos into membrane structures. Both mechanisms are involved in immune regulation and cell survival. However, phagocytosis triggers degradation of extracellular material whereas autophagy engulfs only cytoplasmic elements. Furthermore, activation and maturation of these two processes are different. LAP (LC3-associated phagocytosis) is a form of phagocytosis that uses components of the autophagy pathway. It can eliminate (i) pathogens, (ii) immune complexes, (iii) threatening neighbouring cells, dead or alive, and (iv) cell debris, such as POS (photoreceptor outer segment) and the midbody released at the end of mitosis. Cells have thus optimized their means of elimination of dangerous components by sharing some fundamental elements coming from the two main lysosomal degradation pathways.
    MeSH term(s) Animals ; Autophagy/physiology ; Humans ; Immune Evasion/physiology ; Infections/immunology ; Infections/metabolism ; Infections/pathology ; Macrophages/immunology ; Microtubule-Associated Proteins/physiology ; Phagocytosis/physiology ; Phagosomes/immunology
    Chemical Substances MAP1LC3A protein, human ; Microtubule-Associated Proteins
    Language French
    Publishing date 2019-09-18
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2019129
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Autophagy-Related Proteins Target Ubiquitin-Free Mycobacterial Compartment to Promote Killing in Macrophages.

    Bah, Aïcha / Lacarrière, Camille / Vergne, Isabelle

    Frontiers in cellular and infection microbiology

    2016  Volume 6, Page(s) 53

    Abstract: Autophagy is a lysosomal degradative process that plays essential functions in innate immunity, particularly, in the clearance of intracellular bacteria such as Mycobacterium tuberculosis. The molecular mechanisms involved in autophagy activation and ... ...

    Abstract Autophagy is a lysosomal degradative process that plays essential functions in innate immunity, particularly, in the clearance of intracellular bacteria such as Mycobacterium tuberculosis. The molecular mechanisms involved in autophagy activation and targeting of mycobacteria, in innate immune responses of macrophages, are only partially characterized. Autophagy targets pathogenic M. tuberculosis via a cytosolic DNA recognition- and an ubiquitin-dependent pathway. In this report, we show that non-pathogenic M. smegmatis induces a robust autophagic response in THP-1 macrophages with an up regulation of several autophagy-related genes. Autophagy activation relies in part on recognition of mycobacteria by Toll-like receptor 2 (TLR2). Notably, LC3 targeting of M. smegmatis does not rely on membrane damage, ubiquitination, or autophagy receptor recruitment. Lastly, M. smegmatis promotes recruitment of several autophagy proteins, which are required for mycobacterial killing. In conclusion, our study uncovered an alternative autophagic pathway triggered by mycobacteria which involves cell surface recognition but not bacterial ubiquitination.
    MeSH term(s) Autophagy-Related Proteins/metabolism ; Cell Line ; Humans ; Macrophages/immunology ; Macrophages/microbiology ; Mycobacterium smegmatis/immunology ; Toll-Like Receptor 2/metabolism ; Ubiquitin/metabolism
    Chemical Substances Autophagy-Related Proteins ; TLR2 protein, human ; Toll-Like Receptor 2 ; Ubiquitin
    Language English
    Publishing date 2016
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2016.00053
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The Lipid Virulence Factors of Mycobacterium tuberculosis Exert Multilayered Control over Autophagy-Related Pathways in Infected Human Macrophages

    Aïcha Bah / Merlin Sanicas / Jérôme Nigou / Christophe Guilhot / Catherine Astarie-Dequeker / Isabelle Vergne

    Cells, Vol 9, Iss 3, p

    2020  Volume 666

    Abstract: Autophagy is an important innate immune defense mechanism that controls Mycobacterium tuberculosis ( Mtb ) growth inside macrophages. Autophagy machinery targets Mtb -containing phagosomes via xenophagy after damage to the phagosomal membrane due to the ... ...

    Abstract Autophagy is an important innate immune defense mechanism that controls Mycobacterium tuberculosis ( Mtb ) growth inside macrophages. Autophagy machinery targets Mtb -containing phagosomes via xenophagy after damage to the phagosomal membrane due to the Type VII secretion system Esx-1 or via LC3-associated phagocytosis without phagosomal damage. Conversely, Mtb restricts autophagy-related pathways via the production of various bacterial protein factors. Although bacterial lipids are known to play strategic functions in Mtb pathogenesis, their role in autophagy manipulation remains largely unexplored. Here, we report that the lipid virulence factors sulfoglycolipids (SLs) and phthiocerol dimycocerosates (DIMs) control autophagy-related pathways through distinct mechanisms in human macrophages. Using knock-out and knock-in mutants of Mtb and Mycobacterium bovis BCG (Bacille Calmette Guerin) and purified lipids, we found that (i) Mtb mutants with DIM and SL deficiencies promoted functional autophagy via an MyD88-dependent and phagosomal damage-independent pathway in human macrophages; (ii) SLs limited this pathway by acting as TLR2 antagonists; (iii) DIMs prevented phagosomal damage-independent autophagy while promoting Esx-1-dependent xenophagy; (iv) and DIMs, but not SLs, limited the acidification of LC3-positive Mtb compartments. In total, our study reveals an unexpected and intricate role for Mtb lipid virulence factors in controlling autophagy-related pathways in human macrophages, thus providing further insight into the autophagy manipulation tactics deployed by intracellular bacterial pathogens.
    Keywords autophagy ; mycobacterium ; tuberculosis ; lipids ; macrophage ; phagosome ; lysosomes ; innate immunity ; Biology (General) ; QH301-705.5
    Subject code 571 ; 572
    Language English
    Publishing date 2020-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Autophagy in Mycobacterium tuberculosis and HIV infections.

    Espert, Lucile / Beaumelle, Bruno / Vergne, Isabelle

    Frontiers in cellular and infection microbiology

    2015  Volume 5, Page(s) 49

    Abstract: Human Immunodeficiency Virus (HIV) and Mycobacterium tuberculosis (M.tb) are among the most lethal human pathogens worldwide, each being responsible for around 1.5 million deaths annually. Moreover, synergy between acquired immune deficiency syndrome ( ... ...

    Abstract Human Immunodeficiency Virus (HIV) and Mycobacterium tuberculosis (M.tb) are among the most lethal human pathogens worldwide, each being responsible for around 1.5 million deaths annually. Moreover, synergy between acquired immune deficiency syndrome (AIDS) and tuberculosis (TB) has turned HIV/M.tb co-infection into a major public health threat in developing countries. In the past decade, autophagy, a lysosomal catabolic process, has emerged as a major host immune defense mechanism against infectious agents like M.tb and HIV. Nevertheless, in some instances, autophagy machinery appears to be instrumental for HIV infection. Finally, there is mounting evidence that both pathogens deploy various countermeasures to thwart autophagy. This mini-review proposes an overview of the roles and regulations of autophagy in HIV and M.tb infections with an emphasis on microbial factors. We also discuss the role of autophagy manipulation in the context of HIV/M.tb co-infection. In future, a comprehensive understanding of autophagy interaction with these pathogens will be critical for development of autophagy-based prophylactic and therapeutic interventions for AIDS and TB.
    MeSH term(s) Autophagy ; HIV Infections/immunology ; Humans ; Tuberculosis/immunology
    Language English
    Publishing date 2015
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2015.00049
    Database MEDical Literature Analysis and Retrieval System OnLINE

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