Inflammatory immune modulators of AML lung infiltration and respiratory failure
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE319763 | GEO | 2026/05/22
REPOSITORIES: GEO
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Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
2026-05-22 | GSE275542 | GEO
Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
2026-05-22 | GSE269039 | GEO
Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experiments in vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
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Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
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Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
2026-05-22 | GSE269041 | GEO
Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
2026-05-22 | GSE269040 | GEO
Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experiments in vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
2026-05-22 | GSE316710 | GEO
Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
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Project description:Acute myeloid leukemia (AML) is a blood cancer with poor survival outcomes. Limited studies have reported lethal complications in patients due to leukemia infiltration into solid tissues such as the lung, but the related mechanisms remain understudied. Here, we map the transcriptional landscape of the mouse lung microenvironment at single-cell resolution in the AML-infiltrated lungs. Our analysis demonstrated a considerable remodeling of the lung microenvironment under leukemia conditions, as indicated by expansion of stromal myofibroblasts and reduction of endothelial capillary aerocytes. Those changes were accompanied by changes in immune resident cells of the lung microenvironment, as supported by reduction of B- and T- cell proportions, and increased frequencies of activated neutrophils and monocyte populations. We show an induction of inflammatory response within the microenvironment of the leukemic lung. We dissect the spatial interplay between AML and the lung microenvironment, and we identify previously unappreciated interactions driven by inflammatory mediators within the leukemic milieu. Of note, we show that Lgals9 (encoding for Galectin-9) mediates most of cell-cell interactions within the microenvironment of the AML-infiltrated lungs. LGALS9 is highly expressed in AML patients and its role in AML remains elusive. Targeting Galectin-9 reduces the AML burden in the lungs and reverses the infiltration phenotype. Combining single-cell, spatial transcriptomics approaches and functional experimentsin vivo, our study is the first to characterize the pulmonary infiltration phenotype in AML, opening the route for novel treatment strategies in acute leukemia.
2026-05-22 | GSE269038 | GEO
Project description:Here we asked whether infiltration of leukemic blasts initiated a response that could be detected in the interstitial fluid phase of the spleen in a rat model known to mimic human acute myeloid leukemia (AML). By cannulating efferent lymphatic vessels, we were able to monitor the response of the spleen microenvironment during leukemia development. Flow cytometric analysis of lymphocytes isolated from spleen lymph showed increased STAT3 and CREB signaling, and proteins related to these pathways were identified with a different profile in leukemic when compared with control spleen lymph. Additionally, SPARC-like 1 protein, recently identified as a promoter of AML cell growth and a biomarker of patient outcome, was locally produced in the spleen and upregulated in the leukemic setting. Thus, interstitial fluid, and its surrogate efferent lymph, can be used to provide unique information about spleen responses and substances released to the general circulation during leukemia development.
2023-06-23 | PXD011399 | Pride