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Immature low-density neutrophils exhibit metabolic flexibility that facilitates breast cancer liver metastasis

ABSTRACT: Immature low-density neutrophils exhibit metabolic flexibility that facilitates breast cancer liver metastasis

PROVIDER: PRJNA509476 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8312970_1.fastq.gz	Fastqsanger.gz
	SRR8312970_2.fastq.gz	Fastqsanger.gz
	SRR8312971_1.fastq.gz	Fastqsanger.gz
	SRR8312971_2.fastq.gz	Fastqsanger.gz
	SRR8312972_1.fastq.gz	Fastqsanger.gz

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Immature low-density neutrophils exhibit metabolic flexibility that facilitates breast cancer liver metastasis

Project description:Neutrophils play a key role in the control of metastatic progression. Neutrophils are phenotypically heterogeneous and can exert either anti- or pro-metastatic functions. Here, we demonstrate that tumor cells capable of forming liver metastases induce an accumulation of neutrophils in the peripheral blood and liver parenchyma. Cancer cell-derived G-CSF, in concert with other factors, mobilizes immature low-density neutrophils that promote liver metastasis. In contrast, mature high-density neutrophils inhibit the formation of liver metastases. Transcriptomic and metabolomic analyses of high- and low- density neutrophils reveal engagement of numerous metabolic pathways specifically in low-density neutrophils. Low-density neutrophils exhibit enhanced global bioenergetic capacity, through their ability to engage mitochondrial-dependent ATP production, and remain capable of executing pro-metastatic neutrophil functions, including NETosis, under nutrient-deprived conditions. Together, these data reveal that distinct pro-metastatic neutrophil populations exhibit a high degree of metabolic flexibility, which facilitates metastatic progression and the formation of liver metastases.

2019-06-26 | GSE123669 | GEO

DRUG-seq of high-density neutrophils (HDNs), mature low-density neutrophils (M-LDN), and immature low-density neutrophils (IM-LDN) in patients with colorectal cancer

Project description:High-density neutrophils (HDNs), mature low-density neutrophils (M-LDN), and immature low-density neutrophils (IM-LDN) were isolated from peripheral blood of nine treatment-naïve colorectal cancer (CRC) patients with histologically confirmed diagnoses, followed by gene expression profiling of these neutrophil subsets using Digital RNA with pertUrbation of Genes (DRUG) sequencing.

2025-11-02 | GSE302902 | GEO

DRUG-seq of high-density neutrophils (HDNs), mature low-density neutrophils (M-LDN), and immature low-density neutrophils (IM-LDN) in patients with colorectal cancer

Project description:DRUG-seq of high-density neutrophils (HDNs), mature low-density neutrophils (M-LDN), and immature low-density neutrophils (IM-LDN) in patients with colorectal cancer

| PRJNA1292799 | ENA

Metabolic flexibility and expression of CD98 define the low density neutrophils mobilised in response to G-CSF

Project description:Low density neutrophils (LDN) co-purify with mononuclear cells during density-gradient separation of peripheral blood. LDN are rarely detected in healthy individuals but appear in the peripheral blood (PB) of patients with inflammatory diseases, malignancies and in individuals treated with granulocyte colony-stimulating factor (G-CSF). Using human G-CSF mobilized LDN, this study reveals that LDN are transcriptionally, proteomically and metabolically distinct from other neutrophils. Single Cell RNAseq analysis reveals that LDN from these donors comprise one major population, with multiple interrelated transcriptional states, representing the continuum of neutrophil maturation. LDN can engage both glycolysis and mitochondrial respiration to meet energy demands, which affords increased metabolically flexibility in the nutrient perturbed tissue environments found in tumours and inflammatory diseases. This study also identifies upregulated expression of CD98, a transporter for branch chain and aromatic amino acids, as a cell surface marker for LDN in peripheral blood. CD98 may contribute to the functional properties of LDNs and represents a useful phenotypic marker.

2022-12-19 | PXD023952 | Pride

Maturing Neutrophils of Lower Density Associate with Thrombocytopenia in Puumala Orthohantavirus-Caused Hemorrhagic Fever with Renal Syndrome - Human samples

Project description:Puumala orthohantavirus-caused hemorrhagic fever with renal syndrome (PUUV-HFRS) is characterized by significant neutrophil activation. Neutrophils, the most abundant immune cells in circulation, are equipped to respond rapidly to infections and exhibit a notable heterogeneity. This study aims to identify and characterize different neutrophil subsets in the circulation of PUUV-HFRS patients, focusing on low-density granulocytes (LDGs) and normal density polymorphonuclear cells (PMNs). The study finds that PMNs show activation of antiviral pathways, while circulating LDGs increase following acute PUUV-HFRS. Additionally, PUUV-associated LDGs, primarily immature, likely reflect increased bone marrow neutrophil production. Notably, the frequency of LDGs and a "left shift" in blood are associated with the extent of thrombocytopenia, a hallmark of severe HFRS, suggesting a role for maturing neutrophils in disease pathogenesis. Unlike COVID-19 associated LDGs, PUUV LDGs did not exhibit significant immunosuppressive ability, indicating inherent biological differences in LDG responses based on the causative virus or infection kinetics. RNA sequencing was performed on neutrophils isolated from four cohorts: healthy control PMNs, PUUV-infected PMNs, PUUV-infected CD16- LDGs, and PUUV-infected CD16+ LDGs. The RNA sequencing and subsequent bioinformatics analysis were conducted by the Biomedicum Functional Genomics Unit at the Helsinki Institute of Life Science and Biocenter Finland at the University of Helsinki.

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Dexamethasone modulates immature neutrophils and interferon programming in severe COVID-19

Project description:While critical for host defense, innate immune cells are also pathologic drivers of acute respiratory distress syndrome (ARDS). Innate immune dynamics during COVID-19 ARDS, compared to ARDS from other respiratory pathogens, is unclear. Moreover, mechanisms underlying beneficial effects of dexamethasone during severe COVID-19 remain elusive. Using scRNA-seq and plasma proteomics, we discovered that compared to bacterial ARDS, COVID-19 was associated with expansion of distinct neutrophil states characterized by interferon (IFN) and prostaglandin (PG) signalling. Dexamethasone during severe COVID-19 depleted circulating neutrophils, altered IFNactive neutrophils, downregulated interferon-stimulated gene, and activated IL1R2+ve neutrophils. Dexamethasone also expanded immunosuppressive immature neutrophils and remodeled cellular interactions by changing neutrophils from information receivers into information providers. Male patients had higher proportions of IFNactive neutrophils, preferential steroid-induced immature neutrophil expansion, and possibly different effects on outcome. Our single-cell atlas (www.biernaskielab.ca/COVID_neutrophil) defines COVID-19-enriched neutrophil states and molecular mechanisms of dexamethasone action to develop targeted immunotherapies for severe COVID-19.

2021-10-05 | GSE157789 | GEO

Transcriptomic Profiling of Neutrophils and Low-Density Granulocytes in COVID-19 Patients

Project description:The severity of COVID-19 is linked to excessive inflammation. Neutrophils represent a critical arm of the innate immune response and are major mediators of inflammation, but their role in COVID-19 pathophysiology remains poorly understood. We conducted transcriptomic profiling of neutrophils obtained from patients with mild and severe COVID-19, as well as from non-infected healthy controls. Additionally, low-density granulocytes (LDGs) from patients with severe COVID-19 were included to understand their unique role. Transcriptomic analysis of polymorphonuclear cells (PMNs), consisting mainly of mature neutrophils, revealed a striking type I interferon (IFN-I) gene signature in severe COVID-19 patients, contrasting with mild COVID-19 and healthy controls. LDGs from severe COVID-19 patients exhibited an immature neutrophil phenotype and lacked this IFN-I signature. These findings underscore the crucial role of neutrophil inflammasomes in driving inflammation during severe COVID-19. The study provides insights into the pathological mechanisms of severe COVID-19 and highlights potential targets for therapeutic intervention.

2024-07-23 | GSE272381 | GEO

Transcriptomic profiling of high-density neutrophils in human thyroid cancer.

Project description:We performed transcriptomics analysis on the high-density neutrophils from whole blood of thyroid cancer patients.

2024-04-11 | GSE239976 | GEO

Chil3+ immature neutrophils inhibit anti-tumor immunity and impede immune checkpoint blockade therapy in bone metastases [RNA-Seq]

Project description:Bone metastases remain incurable and respond poorly to immune checkpoint blockade (ICB) therapy. The impact of neutrophil maturation in cancer remains largely unknown, especially in refractory tumors including bone metastases. Here, we observed the predominance of immature neutrophils in the bone metastasis microenvironment of both mouse models and cancer patients. DKK1 induces the immature-like functional state in neutrophils, which exert robust immunosuppressive capabilities to inhibit anti-tumor response of CD8+ T cells. Mechanistically, driven by the DKK1-CKAP4-STAT6 signaling, Chil3 expression is identified and required for the immune suppression mediated by immature neutrophils in bone metastases. Moreover, using multiple syngeneic and human immune system (HIS) mouse models, we found that DKK1 blockade efficiently allows neutrophil maturation to improve the immune microenvironment, controls tumor progression, and enhances ICB therapy response in bone metastases. Thus, our findings uncover an essential role for immature neutrophils in cancer, especially in bone metastases, and propose a potential strategy modulating neutrophils to improve cancer immunotherapy.

2025-06-01 | GSE295537 | GEO

Chil3+ immature neutrophils inhibit anti-tumor immunity and impede immune checkpoint blockade therapy in bone metastases [scRNA-seq]

2025-06-01 | GSE295533 | GEO