Borrelia burgdorferi, the agent of Lyme disease, promotes pro-inflammatory changes in endothelium that lead to the recruitment of leukocytes. The host immune response to infection results in increased levels of IFN-gamma in the serum and lesions of Lyme disease patients that correlate with greater severity of disease. Therefore, the effect of IFN-gamma on the gene expression profile of primary human endothelial cells exposed to B. burgdorferi was determined. B. burgdorferi and IFN-gamma synergistically augmented the expression of 34 genes, seven of which encode chemokines. Six of these (CCL7, CCL8, CX3CL1, CXCL9, CXCL10, and CXCL11) attract T lymphocytes, and one (CXCL2) is specific for neutrophils. Synergistic production of the attractants for T cells was confirmed at the protein level. IL-1beta, TNF-alpha, and LPS also cooperated with IFN-gamma to induce synergistic production of CXCL10 by endothelium, indicating that IFN-gamma potentiates inflammation in concert with a variety of mediators. An in vitro model of the blood vessel wall revealed that an increased number of human T lymphocytes traversed endothelium exposed to B. burgdorferi and IFN-gamma, as compared to unstimulated endothelial monolayers. In contrast, addition of IFN-gamma diminished the migration of neutrophils across B. burgdorferi-activated endothelium. IFN-gamma thus alters gene expression by endothelium exposed to B. burgdorferi in a manner that promotes recruitment of T cells and suppresses that of neutrophils. This modulation may facilitate the development of chronic inflammatory lesions in Lyme disease.
IFN-gamma alters the response of Borrelia burgdorferi-activated endothelium to favor chronic inflammation.
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View SamplesThe goal is to investigate gene regulation in endometrial stromal cells expressing the Notch ligand Jag1.
Notch ligand-dependent gene expression in human endometrial stromal cells.
Specimen part
View SamplesBackground: Human interfollicular epidermis is sustained by the proliferation of stem cells and their progeny, transient amplifying cells. Molecular characterization of these two cell populations is essential for better understanding of self renewal, differentiation and mechanisms of skin pathogenesis. The purpose of this study was to obtain gene expression profiles of alpha 6+/MHCI+, transient amplifying cells and alpha 6+/MHCI- , putative stem cells, and to compare them with existing data bases of gene expression profiles for mouse hair follicle stem cells. The expression of Major Histocompatibility Complex (MHC) class I, previously shown to be absent in stem cells in several tissues, and alpha 6 integrin were used to isolate MHCI positive basal cells , and MHCI low/negative basal cells.
No associated publication
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Integrated genomic analysis of relapsed childhood acute lymphoblastic leukemia reveals therapeutic strategies.
Specimen part, Disease
View SamplesThere is a distinct signature of differentially expressed probes from diagnosis to relapse
Integrated genomic analysis of relapsed childhood acute lymphoblastic leukemia reveals therapeutic strategies.
Specimen part, Disease
View SamplesZIKV alters transcriptional responses of infected cells to avoid immune detection. We have compared the transcriptional responses of ZIKV-infected hBMECs and mock-infected hBMECs.
Zika Virus Persistently Infects and Is Basolaterally Released from Primary Human Brain Microvascular Endothelial Cells.
Specimen part, Time
View SamplesVon Willebrand factor is a paracrine/autocrine regulator of human mesenchymal stem cell adhesion to distressed/apoptotic endothelial cells.
Von willebrand factor increases endothelial cell adhesiveness for human mesenchymal stem cells by activating p38 mitogen-activated protein kinase.
Specimen part
View SamplesWhole body knockout mice lacking IQ-motif containing GTPase-activating protein 2 (IQGAP2) develop spontaneous hepatocellular carcinoma (HCC) at the age of 12 months and older (Schmidt et al., 2008). Hepatic transcript expression profiles were obtained for IQGAP2 knockout and wild-type control mice of two age groups, 6- and 24-month-old. Liver samples from 24-month-old IQGAP2 knockout mice were HCC tumors, livers from all other groups were tumor-free. Results provide insights into the potential role of IQGAP2 as a liver-specific tumor suppressor.
Transcript profiling identifies iqgap2(-/-) mouse as a model for advanced human hepatocellular carcinoma.
Sex, Age, Specimen part
View SamplesDengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). While the mechanisms that lead to vascular permeability are unknown, the endothelium plays a central role in regulating fluid and cellular efflux from capillaries. Thus, dysregulation of endothelial cells functions by dengue virus infection may contribute to pathogenesis and severe disease.
Endothelial cells elicit immune-enhancing responses to dengue virus infection.
Specimen part, Time
View SamplesREST is a master regulator of genes that are involved in the acqusition of neuronal fate. The role of REST is not well understood so we attempted to investigate the role of REST in the development of neural cells by analysing the genes that are upregulated when REST is knocked down via shRNA
REST regulates the pool size of the different neural lineages by restricting the generation of neurons and oligodendrocytes from neural stem/progenitor cells.
Specimen part
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