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Macrophage-derived insulin antagonist ImpL2 induces lipoprotein mobilization upon bacterial infection

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F23%3A00580499" target="_blank" >RIV/60077344:_____/23:00580499 - isvavai.cz</a>

  • Alternative codes found

    RIV/60076658:12310/23:43907144

  • Result on the web

    <a href="https://www.embopress.org/doi/epdf/10.15252/embj.2023114086" target="_blank" >https://www.embopress.org/doi/epdf/10.15252/embj.2023114086</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.15252/embj.2023114086" target="_blank" >10.15252/embj.2023114086</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Macrophage-derived insulin antagonist ImpL2 induces lipoprotein mobilization upon bacterial infection

  • Original language description

    The immune response is an energy-demanding process that must be coordinated with systemic metabolic changes redirecting nutrients from stores to the immune system. Although this interplay is fundamental for the function of the immune system, the underlying mechanisms remain elusive. Our data show that the pro-inflammatory polarization of Drosophila macrophages is coupled to the production of the insulin antagonist ImpL2 through the activity of the transcription factor HIF1 alpha. ImpL2 production, reflecting nutritional demands of activated macrophages, subsequently impairs insulin signaling in the fat body, thereby triggering FOXO-driven mobilization of lipoproteins. This metabolic adaptation is fundamental for the function of the immune system and an individual's resistance to infection. We demonstrated that analogically to Drosophila, mammalian immune-activated macrophages produce ImpL2 homolog IGFBP7 in a HIF1 alpha-dependent manner and that enhanced IGFBP7 production by these cells induces mobilization of lipoproteins from hepatocytes. Hence, the production of ImpL2/IGFBP7 by macrophages represents an evolutionarily conserved mechanism by which macrophages alleviate insulin signaling in the central metabolic organ to secure nutrients necessary for their function upon bacterial infection.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2023

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    EMBO Journal

  • ISSN

    0261-4189

  • e-ISSN

    1460-2075

  • Volume of the periodical

    42

  • Issue of the periodical within the volume

    OCT

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    26

  • Pages from-to

    e114086

  • UT code for WoS article

    001082872700001

  • EID of the result in the Scopus database

    2-s2.0-85173942783