Bone marrow neutropoiesis bias underlies inflammatory comorbidities
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA991451 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25133800_1.fastq.gz | Fastqsanger.gz | |||
| SRR25133800_2.fastq.gz | Fastqsanger.gz | |||
| SRR25134100_1.fastq.gz | Fastqsanger.gz | |||
| SRR25134100_2.fastq.gz | Fastqsanger.gz | |||
| SRR25133801_1.fastq.gz | Fastqsanger.gz |
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Project description:Bone marrow neutropoiesis bias underlies inflammatory comorbidities [multiomics]
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Project description:Local chronic inflammation exacerbates the prevalence and severity of associated distal organ comorbidities, causing catastrophic consequences for patients. However, the underlying mechanisms remain unclear. Here, we found that periodontitis increased the circulating pro-inflammatory neutrophils, which could be easily recruited to rheumatoid arthritis (RA) joints and aggravated articular destruction. Single-cell multiomics sequencing has revealed that periodontitis induces transcriptomic and epigenomic rewiring of hematopoietic stem and progenitor cells (HSPCs), which display skewed differentiation toward the neutrophil lineage, resulting in an increase in pro-inflammatory neutrophils. We further identified that periodontitis-elevated type I interferons are responsible for guiding the continuous neutropoiesis bias in the bone marrow. Resolution of periodontitis can reverse the differentiation bias of HSPCs and alleviate the progression of RA. This study indicated that neutropoiesis bias induces the progression of inflammatory comorbidities and emphasizes the necessity of controlling local chronic inflammation in the management of inflammatory comorbidities.
2025-05-12 | GSE236476 | GEO
Project description:Local chronic inflammation exacerbates the prevalence and severity of associated distal organ comorbidities, causing catastrophic consequences for patients. However, the underlying mechanisms remain unclear. Here, we found that periodontitis increased the circulating pro-inflammatory neutrophils, which could be easily recruited to rheumatoid arthritis (RA) joints and aggravated articular destruction. Single-cell multiomics sequencing has revealed that periodontitis induces transcriptomic and epigenomic rewiring of hematopoietic stem and progenitor cells (HSPCs), which display skewed differentiation toward the neutrophil lineage, resulting in an increase in pro-inflammatory neutrophils. We further identified that periodontitis-elevated type I interferons are responsible for guiding the continuous neutropoiesis bias in the bone marrow. Resolution of periodontitis can reverse the differentiation bias of HSPCs and alleviate the progression of RA. This study indicated that neutropoiesis bias induces the progression of inflammatory comorbidities and emphasizes the necessity of controlling local chronic inflammation in the management of inflammatory comorbidities.
2025-05-12 | GSE236479 | GEO
Project description:Local chronic inflammation exacerbates the prevalence and severity of associated distal organ comorbidities, causing catastrophic consequences for patients. However, the underlying mechanisms remain unclear. Here, we found that periodontitis increased the circulating pro-inflammatory neutrophils, which could be easily recruited to rheumatoid arthritis (RA) joints and aggravated articular destruction. Single-cell multiomics sequencing has revealed that periodontitis induces transcriptomic and epigenomic rewiring of hematopoietic stem and progenitor cells (HSPCs), which display skewed differentiation toward the neutrophil lineage, resulting in an increase in pro-inflammatory neutrophils. We further identified that periodontitis-elevated type I interferons are responsible for guiding the continuous neutropoiesis bias in the bone marrow. Resolution of periodontitis can reverse the differentiation bias of HSPCs and alleviate the progression of RA. This study indicated that neutropoiesis bias induces the progression of inflammatory comorbidities and emphasizes the necessity of controlling local chronic inflammation in the management of inflammatory comorbidities.
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Project description:Bone marrow neutropoiesis bias underlies inflammatory comorbidities [RNA-Seq]
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Project description:This SuperSeries is composed of the SubSeries listed below.
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Project description:Technological advances have greatly improved our knowledge of myelopoiesis, for instance with the discovery of granulocyte-monocyte-DC progenitors (GMDPs), monocyte-DC progenitors (MDPs), common dendritic progenitors (CDPs) and common monocyte progenitors (cMoPs) based on sophisticated flow cytometry approaches. Concomitantly, little progress has been made to characterize the very early phases of human neutropoiesis, despite the recently reported eNePs, PM w/o eNePs, ProNeus, preNeus, all of them being, however, CD66b+neutrophil progenitors. More recently, we identified four SSCloLin-CD66b-CD45dimCD34+/CD34dim/-CD64dimCD115-cells as the earliest precursors specifically committed to the neutrophil lineage present in human bone marrow (BM), which we called neutrophil-committed progenitors (NCPs), namely from NCP1s to NCP4s. In this study, we report the isolation and characterization of two new SSChiCD66b-CD64dimCD115-NCPs that, by phenotypic, flow cytometric SSC, transcriptomic, maturation and immunohistochemistry properties/features, stand after NCP4s but precede the CD66b+Promyelocytes (PMs) during the neutropoiesis cascade. These cells, similarly to SSCloCD45RA+NCP2s/NCP3s and SSCloCD45RA-NCP1s/NCP4s, exhibit phenotypic differences in CD45RA expression levels and, therefore, were named as SSChiCD45RA+NCP5s and SSChiCD45RA-NCP6s. In addition, NCP5s result more immature than NCP6s, as determined by both their cell differentiation and proliferative potential, and by their transcriptomic and phenotypical features. Finally, by examining whether NCPs and all other CD66b+neutrophil precursors are altered in representative hematological malignancies, we found that, in patients with chronic-phase chronic myeloid leukemia (CP-CML), but not with systemic mastocytosis (SM), there is an increased frequency of NCP4s and all downstream neutrophil progenitors, particularly, the CD45RA-cells, like NCP6s, suggesting their involvement in CML pathogenesis. Altogether, our data advance our knowledge of human neutropoiesis.
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Project description:Spot intensity serves as a proxy for gene expression in dual-label microarray experiments. Dye bias is defined as an intensity difference between samples labeled with different dyes attributable to the dyes instead of the gene expression in the samples. Dye bias that is not removed by array normalization can introduce bias into comparisons between samples of interest. But if the bias is consistent across the samples for the same gene, it can be corrected by proper experimental design and analysis. If the dye bias is not consistent across samples for the same gene, but is different for different samples, then removing the bias becomes more problematic, perhaps indicating a technical limitation to the ability of fluorescent signals to accurately represent gene expression. Thus, it is important to characterize dye bias to determine: (1) whether it will be removed for all genes by array normalization, (2) whether it will not be removed by normalization but can be removed by proper experimental design and analysis and (3) whether dye bias correction is more problematic than either of these and is not easily removable. Keywords: dye swap design
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