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Expression data from human alveolar macrophages (AMs) of fetal versus adult origin

ABSTRACT: The impact of cell origin on human lung macrophage identity and function remains unknown. In this study we characterized human alveolar macrophages of fetal versus adult origin. We used microarray to define the gene signatures of human alveolar macrophages derived from CD116+CD64+ fetal monocytes, CD116+CD64- fetal precursors, and CD34+ HSPCs in MISTRG humanized mice.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190257 | GEO | 2021/12/08

REPOSITORIES: GEO

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Expression data from human alveolar macrophages (AMs) of fetal versus adult origin

Project description:Expression data from human alveolar macrophages (AMs) of fetal versus adult origin

| PRJNA786550 | ENA

Expression data from different types of human alveolar macrophage (AM) precursors

Project description:Despite their importance in lung health and disease, it remains unknown how human alveolar macrophages develop early in life. In this study we identified the fetal progenitor of human alveolar macrophages. We used microarray to define the gene signatures of human CD14+ blood monocytes (adult AM precursors), CD116+CD64+ fetal liver monocytes, and CD116+CD64- fetal AM precursors.

2021-12-08 | GSE190256 | GEO

Single-cell RNA-sequencing of human lung monocytes and macrophages from MISTRG mice on day 21 or day 36 post-transplantation with human CD34+ hematopoietic stem and progenitor cells (HSPCs)

Project description:The ontogeny of human lung macrophages derived from blood monocytes is poorly understood. In this study, we employed single-cell RNA-sequencing to investigate the heterogeneity of HSPC-derived human lung monocytes and macrophages in the MISTRG humanized mouse model.

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Capacity of yolk sac macrophages, fetal liver and adult monocytes to colonize an empty niche and develop into functional tissue resident macrophages

Project description:Tissue-resident macrophages can derive from yolk sac macrophages, fetal liver monocytes or adult bone marrow monocytes. Whether these precursors can give rise to transcriptionally identical alveolar macrophages is unknown. Here, we transferred traceable yolk sac macrophages, fetal liver monocytes, adult bone marrow monocytes or adult alveolar macrophages as a control, into the empty alveolar macrophage niche of neonatal Csf2rb-/- mice. All precursors efficiently colonized the alveolar niche and generated alveolar macrophages that were transcriptionally almost identical, with only 22 genes that could be linked to their origin. Underlining the physiological relevance of our findings, all transfer-derived alveolar macrophages self-maintained within the lungs for up to 1 year and durably prevented alveolar proteinosis. Thus, precursor origin does not affect the development of functional self-maintaining tissue-resident macrophages. CD45.1+CD45.2+ yolk sac macrophages, fetal liver monocytes, adult bone marrow monocytes or adult alveolar macrophages from the bronchoalveolar lavage were sorted from wild type CD45.1+CD45.2+ mice of indicated ages. From part of these samples RNA was isolated. The other part was transferred intranasally into the lungs of neonate Csf2rb-/- mice. 6 weeks post-transfer, transfer-derived CD45.1+CD45.2+ alveolar macrophages were sorted from the bronchoalveolar lavage. Wild type CD45.1+CD45.2 alveolar macrophages from the bronchoalveolar lavage of 6 week old mice were sorted as control. 36 samples (arrays) in total. RNA was isolated, amplified with Nugene pico kit, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 1.0 ST Arrays.

2016-03-01 | E-GEOD-76999 | biostudies-arrayexpress

Capacity of yolk sac macrophages, fetal liver and adult monocytes to colonize an empty niche and develop into functional tissue resident macrophages

2016-03-01 | GSE76999 | GEO

Expression data from human alveolar macrophages (AMs)

Project description:Expression data from human alveolar macrophages (AMs)

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Single-cell RNA-sequencing of human vascular and tissue innate lymphoid cells (ILCs) in the spleen of MISTRG humanized mice

Project description:The migratory properties of human ILCs are poorly understood. In this study, we mapped at single-cell resolution the heterogeneity and spatial compartmentalization of human ILCs in the spleen, using an in-vivo model (MISTRG humanized mice) for human ILCs.

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BRAFV600E or mutant MAP2K1 human CD34+ cells establish Langerhans cell-like histiocytosis in immunodeficient mice

Project description:We describe a xenograft model for human LCH-like disease in which we transduced human Cord Blood CD34+ HSPCs with a virus coding for BRAF-V600E - the most abundant pathognomonic somatic mutation occuiring in LCH. Cells were subsequently subjected to RNA-sequencing or transplanted into humanized MISTRG or NSG mice.

2020-10-12 | GSE153831 | GEO

Cell origin dictates programming of resident versus recruited macrophages during acute lung injury

Project description:The primary objective of this study was to compare global differences in transcriptional programming of resident and recruited alveolar macrophages in a time-limited murine model of lung inflammation. We first performed RNA sequencing of the resident and recruited alveolar macrophages from initiation through resolution of LPS-induced lung inflammation in the mouse. Our results indicate that despite existing in a shared environment, cell origin is the major determinant of programming of resident and recruited AMs during an acute inflammatory response. Major areas of difference include cell proliferation, inflammatory cytokine production and metabolism.

2017-09-19 | GSE94749 | GEO

PPARg controls proinflammatory responses in alveolar macrophages

Project description:Tissue resident macrophages are a heterogeneous population with unique functions. During steady state conditions most tissue macrophages are of embryonic origin and maintained locally. Despite their common fetal origin, tissue macrophages are able to fulfil tissue specific functions, suggesting that the local environment can modulate cell function. It has been reported that PPARg is critical for the development of macrophages in the lung. Here, we show that PPARg functions as a transcriptional repressor in alveolar macrophages. Alveolar macrophages lacking Pparg responded more strongly to LPS stimulation by producing more cytokines and phagocytosed more particles in vitro. Certain prostaglandins can act as endogenous ligands for PPARg. We show that prostaglandins were expressed in an organ-specific fashion and modulated cytokine production by alveolar macrophages as well as bone marrow-derived macrophages and monocytic U937 cells. Pparg expression was further induced in macrophages by different cytokine combinations including IL-4, IL-3 and IL-13 suggesting a global role for PPARg which can be regulated by the local environment on two levels. Lastly, repression of inflammatory genes was mediated by PPARg interacting with NFkB and STAT signalling cascades rather than direct transrepression. Therefore PPARg is a modulator of macrophage functions, that changes the inflammatory state of macrophages by regulating classical immune signalling cascades.

2018-03-01 | GSE103102 | GEO

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