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Extracellular Granzyme B directly drives Interferon-stimulated genes expression in macrophages.

ABSTRACT: Previous research indicate MIA propagates maternal inflammation to the fetal developing brain, that manifests as increased pro-inflammatory cytokines and activation of macrophages. Our data sugests that maternal Granzyme B released by aberrant decidual NK cells can reach to the fetal brain and instigate the activation of macrophages. To determine whether Gzmb can directly impact macrophages, we co-cultured murine microglial BV-2 cells with Gzmb for 20 hours, and then performed gene expression profiling analysis. We found that GzmB exposure directly induces a unique gene signature in microglia that includes the unexpected upregulation of multiple interferon-stimulated genes (ISGs).

ORGANISM(S): Mus musculus

PROVIDER: GSE244113 | GEO | 2025/08/01

REPOSITORIES: GEO

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Project description:Activation of the maternal immune system during pregnancy can fetal development, which can lead to postnatal susceptibility to a wide range of diseases, including cardiovascular, metabolic and psychiatric disorders. During maternal immune activation (MIA), the maternal body must balance its ressources between mounting an immune response and investing resources into continued metabolism and growth : both essential for survival of the fetus and a successful pregnancy. How the placenta responds to MIA over time and how it can protect the fetus is not well understood, and neither are the fetal consequences of MIA. Here, we characterised the response to an induced acute inflammation in maternal lungs over time across maternal and fetal organs, using a combination of omics-methods, imaging and integrative computational analysis. We found that the placenta, unlike other maternal organs, did not react by inducing a typical inflammatory response, but instead initially induced genes associated to strengthen tissue integrity and simultaneously reduced growth to prevent exposure to potential infections. Afterwards, a return to homeostasis was observed, with heightened biosynthesis and expression of endoplasmic reticulum (ER) stress genes. This mechanism likely protects the fetus from inflammation, as we observed no immune response in the fetal liver transcriptome. Instead, we observed metabolic adaptations in the fetus, including a release of docosahexaenoic acid (DHA) Notably, DHA has a crucial function for fetal brain development , and levels of triglyceride and phosphatidylcholine lipids that are necessary for transportation of DHA to the brain were also increased. This metabolic response is likely a combination of the placental MIA response and temporary maternal fasting, caused by MIA-induced fever and lack of nutrient intake. Our study shows, for the first time, the temporal and systemic response to MIA in lungs across maternal and fetal organs.

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Extracellular Granzyme B directly drives Interferon-stimulated genes expression in macrophages.

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