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Polarization of Macrophages in Insects: Opening Gates for Immuno-Metabolic Research

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60076658%3A12310%2F21%3A43903808" target="_blank" >RIV/60076658:12310/21:43903808 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.frontiersin.org/articles/10.3389/fcell.2021.629238/full" target="_blank" >https://www.frontiersin.org/articles/10.3389/fcell.2021.629238/full</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3389/fcell.2021.629238" target="_blank" >10.3389/fcell.2021.629238</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Polarization of Macrophages in Insects: Opening Gates for Immuno-Metabolic Research

  • Original language description

    Insulin resistance and cachexia represent severe metabolic syndromes accompanying a variety of human pathological states, from life-threatening cancer and sepsis to chronic inflammatory states, such as obesity and autoimmune disorders. Although the origin of these metabolic syndromes has not been fully comprehended yet, a growing body of evidence indicates their possible interconnection with the acute and chronic activation of an innate immune response. Current progress in insect immuno-metabolic research reveals that the induction of insulin resistance might represent an adaptive mechanism during the acute phase of bacterial infection. In Drosophila, insulin resistance is induced by signaling factors released by bactericidal macrophages as a reflection of their metabolic polarization toward aerobic glycolysis. Such metabolic adaptation enables them to combat the invading pathogens efficiently but also makes them highly nutritionally demanding. Therefore, systemic metabolism has to be adjusted upon macrophage activation to provide them with nutrients and thus support the immune function. That anticipates the involvement of macrophage-derived systemic factors mediating the inter-organ signaling between macrophages and central energy-storing organs. Although it is crucial to coordinate the macrophage cellular metabolism with systemic metabolic changes during the acute phase of bacterial infection, the action of macrophage-derived factors may become maladaptive if chronic or in case of infection by an intracellular pathogen. We hypothesize that insulin resistance evoked by macrophage-derived signaling factors represents an adaptive mechanism for the mobilization of sources and their preferential delivery toward the activated immune system. We consider here the validity of the presented model for mammals and human medicine. The adoption of aerobic glycolysis by bactericidal macrophages as well as the induction of insulin resistance by macrophage-derived factors are conserved between insects and mammals. Chronic insulin resistance is at the base of many human metabolically conditioned diseases such as non-alcoholic steatohepatitis, atherosclerosis, diabetes, and cachexia. Therefore, revealing the original biological relevance of cytokine-induced insulin resistance may help to develop a suitable strategy for treating these frequent diseases.

  • 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

    S - Specificky vyzkum na vysokych skolach

Others

  • Publication year

    2021

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Frontiers in Cell and Developmental Biology

  • ISSN

    2296-634X

  • e-ISSN

  • Volume of the periodical

    9

  • Issue of the periodical within the volume

    FEB 15 2021

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    20

  • Pages from-to

  • UT code for WoS article

    000623210100001

  • EID of the result in the Scopus database

    2-s2.0-85101906386