This SuperSeries is composed of the SubSeries listed below.
The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.
Specimen part
View SamplesMice deficient in MBD2 (Mbd2-/-) were treated with 2% dextran sulfate sodium or normal drinking water for 6 continuous days. A single cell suspension of colon lamina propria and epithelium was isolated, with monocytes (CD11b+ Ly6CHi, MHC-II+/-), macrophages (CD11b+ Ly6C-MHC-II+), cDC2s (CD11b- CD11c+ CD103+) and epithelial cells (CD45- EpCAM+) purified by FACS.
The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.
Specimen part
View SamplesMice deficient in MBD2 (Mbd2-/-) were treated with 2% dextran sulfate sodium or normal drinking water for 6 continuous days. A single cell suspension of colon lamina propria and epithelium was isolated, with monocytes (CD11b+ Ly6CHi, MHC-II+/-), macrophages (CD11b+ Ly6C-MHC-II+), cDC2s (CD11b- CD11c+ CD103+) and epithelial cells (CD45- EpCAM+) purified by FACS.
The Methyl-CpG-Binding Protein Mbd2 Regulates Susceptibility to Experimental Colitis via Control of CD11c<sup>+</sup> Cells and Colonic Epithelium.
Specimen part
View SamplesInsults to the cerebral cortex, such as trauma, ischemia or infections, may result in the development of epilepsy, one of the most common neurological disorders. Previous studies have suggested that perturbations in neurovascular integrity and breakdown of the blood-brain barrier (BBB) lead to neuronal hypersynchronization and epileptiform activity, but the underlying mechanisms are unknown. As with BBB opening, treatment with albumin or with TGF-1 results in the development of hypersynchronized epileptiform activity. Given the latent period before the appearance of epileptiform activity, we hypothesized the underlying mechanism is a transcriptional response which would be similar for BBB breakdown and exposure to albumin or TGF-1. In search of a common pathway and transcriptional activation pattern we performed a genome wide analysis. Genomic expression analyses demonstrated similar expression patterns for BBB opening, albumin and TGF-1 exposure. Most importantly, TGF- pathway blockers suppressed most albumin-induced transcriptional changes.
Astrocytic dysfunction in epileptogenesis: consequence of altered potassium and glutamate homeostasis?
Sex
View SamplesMicroRNAs (miRNAs) are a class of short non-coding RNA that play important roles in disease processes in animals and are present in a highly stable cell-free form in body fluids. Here we examine the capacity of host and parasite miRNAs to serve as tissue or serum biomarkers of Schistosoma mansoni infection. Sequencing of small RNAs from serum confirmed the presence of miRNAs and revealed 11 parasite-derived miRNAs that were detectable by 8 weeks post S.mansoni infection. Overall design: Small RNA content in serum of naïve and Schistosoma mansoni infected mice were examined in two different librarys. 1- prepared according to the 290 Illumina small RNA Sample Preparation Kit version 1.5 and sequenced on the GAIIX and 2- prepared according to the TruSeq Small RNA protocol (without size-selecting small 295 RNA) and sequenced on the HiSeq2
Parasite-derived microRNAs in host serum as novel biomarkers of helminth infection.
Sex, Cell line, Subject
View SamplesWe aimed to identify the gene network and pathway biology associated with neonatal sepsis by determining genome-wide alterations in host RNA in infected infants
Identification of a human neonatal immune-metabolic network associated with bacterial infection.
Sex, Specimen part
View SamplesFine control of macrophage activation is required to prevent inflammatory disease, particularly at barrier sites such as the lung. However, the dominant mechanisms that regulate pulmonary MFs during inflammation are currently poorly understood. Here we show that airway MFs are substantially less able to respond to the canonical type-2 cytokine IL-4, which underpins allergic disease and parasite worm infections, than lung tissue or peritoneal cavity MFs. We reveal that MF hypo-responsiveness to IL-4 is dictated by the lung environment, though independent of the host microbiota or the prominent lung extracellular matrix components surfactant protein D and mucin 5b. Rather, compared to cavity MFs, airway MFs display severely dysregulated metabolism. Strikingly, upon removal from the lung, alveolar MFs regain IL-4 responsiveness in a process dependent upon glycolysis. Thus, we propose that impaired glycolysis within the pulmonary niche is a central determinant for regulation of MF responsiveness during type-2 inflammation. Overall design: The 13 analysed samples belong to 6 different groups, each group consisted of 2 or 3 samples. The groups consist of 3 separate macrophage populations, from either control or IL-4 complex treated mice. Each individual sample was generated from 3-5 pooled biological replicate mice.
The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation.
Treatment, Subject
View SamplesS. reilianum triggered loss of organ and meristem identity, and loss of meristem determinacy in male and female inflorescences and flowers. Microarray analysis showed that these developmental changes were accompanied with transcriptional regulation of genes proposed to regulate floral organ and meristem identity, and meristem determinacy in maize.
Sporisorium reilianum infection changes inflorescence and branching architectures of maize.
Specimen part, Time
View SamplesCD133-positive colorectal cancer cells exhibit enhanced tumorigenicity over CD133-negative cells. The CD133+ cells are more interactive with and responsive to their stromal microenvironment because they also express the cognate receptors, such as CXCR4, for ligands produced by their neighboring carcinoma-associated fibroblasts, such as SDF-1 (stromal-derived growth factor).
CD133+ colon cancer cells are more interactive with the tumor microenvironment than CD133- cells.
Specimen part, Disease, Disease stage
View Samples6-8 week old BL6, FVB/N and SV129 mouse strains were kept in normoxia or hypobaric hypoxia for 4 weeks and then phenotyped by echocardiogram and right ventricular heart catheterization, followed by tissue collection. In addition, Affymetrix expression analysis was conducted in a paired fashion.
Murine pulmonary response to chronic hypoxia is strain specific.
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