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The effect of beta-glucan - induced trained immunity on the transcriptomic profile of bone marrow granulocyte-macrophage progenitors (GMP) in tumor-bearing mice

ABSTRACT: The effect of beta-glucan - induced trained immunity on the transcriptomic profile of bone marrow granulocyte-macrophage progenitors (GMP) in tumor-bearing mice

PROVIDER: PRJNA579922 | ENA |

REPOSITORIES: ENA

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The effect of beta-glucan - induced trained immunity on the transcriptomic profile of bone marrow granulocyte-macrophage progenitors (GMP) in tumor-bearing mice

Project description:Induction of trained immunity by beta-glucan has been shown to promote transcriptomic alterations in myeloid cells. Progenitors in the bone marrow are also affected by trained immunity and also regulate anti-tumor immune responses . In this study, we performed RNA sequencing in GMP from tumor-bearing mice in order to investigate the impact of trained immunity on the transcriptomic profile of myeloid progenitors in the tumor setting.

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Project description:Trained immunity is the heightened state of innate immune memory that enhances immune response resulting in nonspecific protection. Epigenetic changes and metabolic reprogramming are critical steps that regulate trained immunity. In this study, we reported the involvement of O6-methylguanine DNA methyltransferase (MGMT), a DNA repair enzyme of lesion induced by alkylating agents, in regulation the trained immunity induced by β-glucan (BG). Pharmacological inhibition or silencing of MGMT expression altered LPS stimulated pro-inflammatory cytokine productions in BG-trained bone marrow derived macrophages (BMMs). Targeted deletion of Mgmt in BMMs resulted in reduction of the trained responses both in vitro and in vivo models. The transcriptomic analysis revealed that the dampening trained immunity in MGMT KO BMMs is partially mediated by ATM/FXR/AMPK axis affecting the MAPK/mTOR/HIF1α pathways and the reduction in glycolysis function. Taken together, a failure to resolve a DNA damage may have consequences for innate immune memory.

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