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Danio rerio
4 Downloadable Samples
IlluminaHiSeq2500
Description
The microenvironment is an important regulator of hematopoietic stem and progenitor cell (HSPC) biology. Interactions between the niche and stem cells have been difficult to track, but recent advances marking fluorescent HSPCs have allowed exquisite visualization in the caudal hematopoietic tissue (CHT) of the developing zebrafish. Sinusoidal endothelial cells interact closely with HSPCs as they colonize this niche. Here we show that the chemokine cxcl8 and its receptor, cxcr1, are abundantly expressed by zebrafish endothelial cells and we identify cxcl8/cxcr1 signaling as a positive regulator of HSPC colonization using genetic gain- and loss-of-function techniques. Single-cell tracking experiments demonstrated that this effect is due to an increase in HSPC “cuddling” by endothelial cells, thereby increasing CHT residency time and allowing more HSPC cell divisions to occur. Enhanced cxcl8/cxcr1 signaling was associated with an increase in the volume of the CHT and induction of cxcl12a expression, favoring HSPC colonization. Finally, using parabiotic zebrafish, we show that cxcr1 acts stem cell non-autonomously to improve the efficiency of donor HSPC engraftment. This work identifies a mechanism by which the hematopoietic niche remodels to promote HSPC engraftment and suggests that cxcl8/cxcr1 signaling is a potential therapeutic target in patients undergoing hematopoietic stem cell transplantation. Overall design: Kdrl:mcherry and kdrl:mcherry;kdrl:cxcr1 zebrafish were dissociated and endothelial cells purified by FACS. RNA-seq libraries were prepared from endothelial cells purified from two independent clutches of fish (four libraries total).
Publication Title
CXCR1 remodels the vascular niche to promote hematopoietic stem and progenitor cell engraftment.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 2 Downloadable Samples
- Illumina HiSeq 2500
Description
The microenvironment is an important regulator of hematopoietic stem and progenitor cell (HSPC) biology. Interactions between the niche and stem cells have been difficult to track, but recent advances marking fluorescent HSPCs have allowed exquisite visualization in the caudal hematopoietic tissue (CHT) of the developing zebrafish. Sinusoidal endothelial cells interact closely with HSPCs as they colonize this niche. Here we show that the chemokine cxcl8 and its receptor, cxcr1, are abundantly expressed by zebrafish endothelial cells and we identify cxcl8/cxcr1 signaling as a positive regulator of HSPC colonization using genetic gain- and loss-of-function techniques. Single-cell tracking experiments demonstrated that this effect is due to an increase in HSPC “cuddling” by endothelial cells, thereby increasing CHT residency time and allowing more HSPC cell divisions to occur. Enhanced cxcl8/cxcr1 signaling was associated with an increase in the volume of the CHT and induction of cxcl12a expression, favoring HSPC colonization. Finally, using parabiotic zebrafish, we show that cxcr1 acts stem cell non-autonomously to improve the efficiency of donor HSPC engraftment. This work identifies a mechanism by which the hematopoietic niche remodels to promote HSPC engraftment and suggests that cxcl8/cxcr1 signaling is a potential therapeutic target in patients undergoing hematopoietic stem cell transplantation. Overall design: Primary human endothelial cells were serum starved for 12 hours followed by treatment with recombinant human CXCL8 or vehicle control for 6 hours. Total RNA was collected from biological duplicates and RNA-seq libraries were prepared.
Publication Title
CXCR1 remodels the vascular niche to promote hematopoietic stem and progenitor cell engraftment.
Sample Metadata Fields
Specimen part, Subject
View Samples
SRP122528- Homo sapiens
- 32 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
RNA Sequencing of human adipose tissue before and after diet-induced weight loss Overall design: Prospective cohort study https://academic.oup.com/jes/article/1/6/625/3754346/Effects-of-Rapid-Weight-Loss-on-Systemic-and?searchresult=1
Publication Title
Fecal microbiota and bile acid interactions with systemic and adipose tissue metabolism in diet-induced weight loss of obese postmenopausal women.
Sample Metadata Fields
Sex, Specimen part, Subject, Time
View Samples- Mus musculus
- 28 Downloadable Samples
- Illumina HiSeq 2000
Description
We previously found that mice deficient in the CD susceptibility gene Nod2 develop small intestinal abnormalities including impaired mucus production by goblet cells and susceptibility to injury, which were associated with interferon-gamma producing intraepithelial lymphocytes. These abnormalities were caused by a striking expansion of a common member of the microbiota, Bacteroides vulgatus. Remarkably, infection of Nod2-deficient mice with the helminth Trichuris muris led to a TH2 response that eliminated B. vulgatus colonization and intestinal abnormalities. In addition, treatment with recombinant IL13 (rIL13) or recombinant IL4 reduced B. vulgatus levels and eliminated goblet cell defects, suggesting that type 2 cytokines alone can reverse intestinal abnormalities in the absence of helminth infection. To determine the mechanism by which type 2 cytokines protected Nod2-/- mice from intestinal abnormalities, we performed RNA-seq on small intestinal tissue from WT, Nod2-/- and rIL13 treated Nod2-/- mice. We found that rIL13 treatment induced a wound healing response characterized by M2 macrophage activation genes. Hence, type 2 cytokines can reverse inflammatory imbalances in the composition of the gut microbiota that occurs in a genetically susceptible host. Overall design: Comparison of small intestinal transcriptome in WT, Nod2-/-, and rIL-13 treated Nod2-/- mice.
Publication Title
Helminth infection promotes colonization resistance via type 2 immunity.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 19 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Mus musculus
- 24 Downloadable Samples
- Illumina HiSeq 2500
Description
Acquisition of the intestinal microbiota begins at birth, and a stable microbial community develops from a succession of key organisms. Disruption of the microbiota during maturation by low-dose antibiotic exposure can alter host metabolism and adiposity. We now show that low-dose penicillin (LDP), delivered from birth, induces metabolic alterations and affects ileal expression of genes involved in immunity. LDP that is limited to early life transiently perturbs the microbiota, which is sufficient to induce sustained effects on body composition, indicating that microbiota interactions in infancy may be critical determinants of long-term host metabolic effects. In addition, LDP enhances the effect of high-fat diet induced obesity. The growth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that the altered microbiota, not antibiotics per se, play a causal role. These studies characterize important variables in early-life microbe-host metabolic interaction and identify several taxa consistently linked with metabolic alterations. Overall design: Male and female mice were exposed to low-dose penicillin from birth. In a second experiment, microbiota from female control and LDP mice was transferred to 3-week old female germ-free mice. Livers were collected at 8 weeks of age, RNA was extracted, and transcriptional differences were measured by RNAseq.
Publication Title
Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Acquisition of the intestinal microbiota begins at birth, and a stable microbial community develops from a succession of key organisms. Disruption of the microbiota during maturation by low-dose antibiotic exposure can alter host metabolism and adiposity. We now show that low-dose penicillin (LDP), delivered from birth, induces metabolic alterations and affects ileal expression of genes involved in immunity. LDP that is limited to early life transiently perturbs the microbiota, which is sufficient to induce sustained effects on body composition, indicating that microbiota interactions in infancy may be critical determinants of long-term host metabolic effects. In addition, LDP enhances the effect of high-fat diet induced obesity. The growth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that the altered microbiota, not antibiotics per se, play a causal role. These studies characterize important variables in early-life microbe-host metabolic interaction and identify several taxa consistently linked with metabolic alterations.
Publication Title
Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences.
Sample Metadata Fields
Sex, Age, Treatment
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Acquisition of the intestinal microbiota begins at birth, and a stable microbial community develops from a succession of key organisms. Disruption of the microbiota during maturation by low-dose antibiotic exposure can alter host metabolism and adiposity. We now show that low-dose penicillin (LDP), delivered from birth, induces metabolic alterations and affects ileal expression of genes involved in immunity. LDP that is limited to early life transiently perturbs the microbiota, which is sufficient to induce sustained effects on body composition, indicating that microbiota interactions in infancy may be critical determinants of long-term host metabolic effects. In addition, LDP enhances the effect of high-fat diet induced obesity. The growth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that the altered microbiota, not antibiotics per se, play a causal role. These studies characterize important variables in early-life microbe-host metabolic interaction and identify several taxa consistently linked with metabolic alterations.
Publication Title
Altering the intestinal microbiota during a critical developmental window has lasting metabolic consequences.
Sample Metadata Fields
Sex, Age, Treatment
View Samples- Mus musculus
- 5 Downloadable Samples
- Illumina HiSeq 2500
Description
Purpose: The gastric microbe Helicobacter pylori represents an ancestral constituent of the human microbiota that causes gastric disorders on the one hand, and is inversely associated with allergies and chronic inflammatory conditions on the other. This study aims to investigate the consequences of trans-maternal exposure to H. pylori extract in utero and during lactation on the regulatory T-cell transcriptome profile. Experiment type: Expression profiling by high throughput sequencing Overall design: Transcriptome profling (RNA-seq) of lung regulatory T-cells in mice after perinatal PBS and H. pylori extract exposure. One factorial design with 2 levels (with and without H. pylori exposure) including 2-3 biological replicates per experimental group. A biological replicate represents pools from 3-4 animals.
Publication Title
Transmaternal Helicobacter pylori exposure reduces allergic airway inflammation in offspring through regulatory T cells.
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 16 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The zinc finger factor Insm1 is known to regulate differentiation of pancreatic cells during development, Here we show that Insm1 is essential for the maintenance of functionally mature pancreatic cells in mice.
Publication Title
Insm1 cooperates with Neurod1 and Foxa2 to maintain mature pancreatic β-cell function.
Sample Metadata Fields
No sample metadata fields
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