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Heme exposure shifts shifts myeloid differentiation in bone marrow derived mixed cell cultures.

ABSTRACT: Heme exposure shifts shifts myeloid differentiation in bone marrow derived mixed cell cultures.

PROVIDER: PRJNA743342 | ENA |

REPOSITORIES: ENA

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Heme exposure shifts shifts myeloid differentiation in bone marrow derived mixed cell cultures.

Project description:Heme is an erythrocyte-derived toxin that drives disease progression in hemolytic anemias. During hemolysis, specialized bone marrow-derived macrophages with a high heme-metabolism capacity orchestrate disease adaptation by removing damaged erythrocytes and heme-protein complexes from the blood and supporting iron recycling for erythropoiesis. Here, we performed single-cell RNA sequencing with RNA velocity analysis of GM-CSF-supplemented mouse bone marrow cultures to assess myeloid differentiation under heme stress. We found that heme-activated NRF2 signaling shifted the differentiation trajectories of cells towards antioxidant, iron-recycling macrophages at the expense of dendritic cells, as these cells were selectively deficient in heme-exposed bone marrow cultures. Heme eliminated the capacity of GM-CSF-supplemented bone marrow cultures to activate antigen-specific T cells. The generation of functionally competent dendritic cells was restored by NRF2 loss. The heme-induced phenotype was reproduced in hemolytic mice with sickle cell disease and spherocytosis and associated with reduced dendritic cell functions in the spleen. Our data provide a novel mechanistic underpinning how hemolytic stress may provoke hyposplenism-related secondary immunodeficiency, which is a critical determinant of mortality in patients with genetic hemolytic anemias.

2022-01-25 | GSE179362 | GEO

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Project description:Inflammatory macrophage activation is a critical component of the antitumor immune response and an emerging therapeutic concept. To evaluate the impact of heme exposure on antitumoral macrophage activity, we grew spheroids of mixed GFP-MC38 and BMDMs that were either untreated or pretreated with heme, INFγ, or heme + INFγ, and characterized them by scRNA-seq.

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