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Streptococcus agalactiae induced gene expression in human coronar artery endothelial cells

ABSTRACT: Early onset sepsis due to Group B streptococcus (GBS) leads to neonatal morbidity, increased mortality and long term neurological deficencies. Interaction between septicemic GBS and confluent monlayers of human coronary artery endothelial cells (HCAEC) was analyzed by a genome wide expression profiling. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real Time RT-PCR assay (Granulocyte chemotactic protein 2 (CXCL6)), ELISA (Urokinase, Cyclooxygenase 2 (COX2), Granulocyte chemotactic protein 1 (IL8)) and Western Blotting (Heme oxygenase1, BCL2 interacting protein (BIM)) at various time points between 4 and 24 hours. In total, 124 genes were differentially regulated (89 upregulated, 35 downregulated) based on a more than 3-fold difference to unstimulated HCAEC. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, infection and inflammation. We confirmed upregulation of urokinase (UPA), COX2, HMOX1 and BCL2 interacting protein and downregulation of CXCL6 and IL8. These results indicate that GBS infection might lead to impaired function of the innate immune system and might contribute to hemorrhagic and inflammatory complications during GBS sepsis. Keywords: stimulated HCAEC (with S. agalactiae) vs unstimulated control cells total samples analysed are 2, including control

ORGANISM(S): Homo sapiens

SUBMITTER: Claudia Beyrich

PROVIDER: E-GEOD-15495 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Streptococcus agalactiae induced gene expression in human coronar artery endothelial cells

Project description:Early onset sepsis due to Group B streptococcus (GBS) leads to neonatal morbidity, increased mortality and long term neurological deficencies. Interaction between septicemic GBS and confluent monlayers of human coronary artery endothelial cells (HCAEC) was analyzed by a genome wide expression profiling. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real Time RT-PCR assay (Granulocyte chemotactic protein 2 (CXCL6)), ELISA (Urokinase, Cyclooxygenase 2 (COX2), Granulocyte chemotactic protein 1 (IL8)) and Western Blotting (Heme oxygenase1, BCL2 interacting protein (BIM)) at various time points between 4 and 24 hours. In total, 124 genes were differentially regulated (89 upregulated, 35 downregulated) based on a more than 3-fold difference to unstimulated HCAEC. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, infection and inflammation. We confirmed upregulation of urokinase (UPA), COX2, HMOX1 and BCL2 interacting protein and downregulation of CXCL6 and IL8. These results indicate that GBS infection might lead to impaired function of the innate immune system and might contribute to hemorrhagic and inflammatory complications during GBS sepsis. Keywords: stimulated HCAEC (with S. agalactiae) vs unstimulated control cells

2010-12-31 | GSE15495 | GEO

Gene expression in human endothelial cell with innate immunity stimulation

Project description:This is an investigation of whole genome gene expression level in human coronary endothelial cells (HCAEC) and human pulmonary endothelial cells (HPAEC) stimulated by FK565 or LipidA. We show that parenteral administration of a pure synthetic Nod1 ligand, FK565, induces site-specific vascular inflammation in mice, which is prominent in and aortic root including aortic valves, slight in aorta and absent in other arteries. The in vitro production of proinflammatory chemokine/cytokine by FK565 is higher in HCAEC than in HPAEC, suggesting that site-specific vascular inflammation is at least in part ascribed to an intrinsic nature of the vascular cell itself. A six chip study using total RNA recovered from HCAEC and HPAEC which were stimulated by LipidA or FK565 in vitro. HCAEC and HPAEC were stimulated with FK565 (10µg/mL) or LipidA (100ng/mL) for 24 hours in 12-well plates (10,000 cells/cm2). Total RNA was extracted and subjected to RNA microarray analysis.

2011-03-01 | E-GEOD-20929 | biostudies-arrayexpress

Physiological profile of the coronary artery and internal thoracic artery endothelial cells as a basis for the structural and functional congrunce of the arterio-arterial continuum

Project description:Currently, it is well established that human endothelial cells (ECs) are characterised by a significant heterogeneity between distinct blood vessels, e.g., arteries, veins, capillaries, and lymphatic vessels. Further, even ECs belonging to the same lineage but grown under different flow patterns (e.g., laminar and oscillatory or turbulent flow) ostensibly have distinct molecular profiles defining their physiological behaviour. Human coronary artery endothelial cells (HCAEC) and human internal thoracic artery endothelial cells (HITAEC) represent two cell lines inhabiting atheroprone and atheroresistant blood vessels (coronary artery and internal thoracic artery, respectively). Resistance of the internal mammary artery to atherosclerosis has been largely attributed to the protective phenotype of HITAEC which reportedly produce higher amounts of vasodilators including nitric oxide (NO) through the respective signaling pathways. However, this hypothesis has not been adequately addressed hitherto as proteomic profiling of HCAEC and HITAEC in a head-to-head comparison setting has not been performed.

2023-10-17 | PXD037861 | Pride

CiaR Transcriptome in Streptococcus agalactiae

Project description:Regulation of gene expression in response to variable and often adverse environmental conditions is an essential component of microbial pathogenesis. We identified the two-component regulatory system CiaRH in a screen for genes essential for the survival of Streptococcus agalactiae (Group B Streptococcus, GBS) on exposure to in vitro models of environmental stress. We constructed site-directed, non-polar deletion mutations in the regulator gene ciaR and compared the growth of CiaR mutant GBS to wild-type GBS under stressed conditions. CiaR mutant GBS are more sensitive than wild-type GBS to elevated temperature, low pH, chemical mutagens and ultraviolet light; the mutants are also more sensitive to cell-wall active antibiotics and antimicrobial peptides. CiaR mutant strains are markedly attenuated in a mouse model of GBS sepsis. To determine the genes regulated by CiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to CiaR mutant GBS under non-stressed conditions.

2012-11-18 | GSE14569 | GEO

LiaR Transcriptome in Streptococcus agalactiae

Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of early-onset neonatal bacterial infection. Evasion of innate immune defenses is critical to neonatal GBS disease pathogenesis. Effectors of the innate immune system such as antimicrobial peptides, as well as numerous antibiotics, target the peptidoglycan layer of the gram positive bacterial cell wall. The intramembrane-sensing histidine kinase class of two-component regulatory systems has recently been identified as important to the gram-positive response to cell wall stress. We identified and characterized the GBS homolog of LiaR, the response regulator component of the LiaFSR system and constructed site-directed, non-polar deletion mutations in the regulator gene liaR. GBS LiaR deletion mutant strains are more susceptible to cell wall active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (colistin, nisin and the human cathelicidin LL-37) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and GBS pneumonia. To determine the genes regulated by LiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to LiaR mutant GBS under non-stressed conditions.

2012-11-18 | GSE14571 | GEO

LiaR Transcriptome in Streptococcus agalactiae

2012-11-18 | E-GEOD-14571 | biostudies-arrayexpress

Transcription profiling of Streptococcus agalactiae strains 2603V/R and 515 and CsrR or CsrS isogenic mutants to better understand the CsrRS regulon

Project description:CsrRS is a two-component regulatory system that controls expression of multiple genes and affects virulence in group B Streptococcus (GBS), a major cause of neonatal sepsis and of invasive infection in chronically ill adults. To better understand the CsrRS regulon and its importance in GBS pathogenicity, we used GBS genomic microarrays to compare global gene expression in GBS strains 2603V/R and 515 with that in CsrR or CsrS isogenic mutants. These results and comparison with data reported previously for GBS strain NEM316 demonstrated a conserved CsrRS regulon of approximately 30 genes including those encoding beta-hemolysin, CAMP factor, and C5a-peptidase, as well as a variable repertoire of genes regulated in one or two of the three strains. Inactivation of CsrS had a similar but weaker effect at most regulated loci, but, in some cases, resulted in more pronounced or divergent regulation compared to CsrR. We conclude that CsrRS regulates a core group of genes including important virulence factors in diverse strains of GBS, but also displays marked variability in the repertoire of regulated genes and in the relative effects of CsrS signaling on CsrR-mediated gene regulation. Such variation is likely to play an important role in strain-specific adaptation of GBS to particular host environments and pathogenic potential in susceptible hosts.

2008-11-25 | E-TIGR-131 | biostudies-arrayexpress

Transcriptome of senescent and non-senescent cells within PanIN pancreatic premalignant lesions in a KRas-driven mouse model

Project description:Cellular senescence is a central barrier to tumorigenesis, acting to block the proliferation of premalignant cells. However, senescent cells residing within tumor lesions can also exert paracrine effects influencing tumor growth and progression. Premalignant pancreatic intraepithelial neoplasia (PanIN) lesions contain senescent cells, yet whether these influence disease progression is unknown. Here we report that senescent cells in PanINs that develop in a Kras-driven mouse model express a pro-inflammatory gene signature, which includes high Cox2 levels. Pharmacologic Cox2 inhibition caused a dramatic reduction in PanIN growth. Senolytic treatment with the Bcl2-family inhibitor ABT-737 reduced the numbers of Cox2-expressing PanIN cells and blocked PanIN formation and progression to carcinoma. These findings indicate that senescent PanIN cells support tumor growth and progression through Cox2 activity, representing crosstalk between interspersed senescent and dividing premalignant cells. Targeted elimination of senescent cells may thus be effective in limiting progression of precancerous lesions.

2021-02-17 | GSE128319 | GEO

High EMT signature score of invasive non-small cell lung cancer (NSCLC) cells correlates with NFĸB driven colony-stimulating factor 2 (CSF2/GM-CSF) secretion by neighboring stromal fibroblasts

Project description:We established co-cultures of invasive or non-invasive NSCLC cell lines and various types of fibroblasts (FBs) to more precisely characterize the molecular mechanism of tumor-stroma crosstalk in lung cancer Differential expression analysis of the respective mono- and co-cultures revealed an upregulation of NFκB-related genes exclusively in co-cultures with Calu-1. Cytokine Array- and ELISA-based characterization of the “cytokine fingerprints” identified CSF2 (GM-CSF), CXCL1, CXCL6, VEGF, IL6, RANTES and IL8 as being specifically upregulated in various co-cultures

2015-03-16 | GSE66616 | GEO

Group B Streptococcus drives major transcriptomic changes in the colonic epithelium

Project description:Group B Streptococcus (GBS) is a leading cause of infant sepsis worldwide. Colonization of the gastrointestinal tract is a critical precursor to late-onset disease in exposed newborns. Neonatal susceptibility to GBS intestinal translocation stems from intestinal immaturity; however, the mechanisms by which GBS exploits the immature host remain unclear. β-hemolysin/cytolysin (βH/C) is a highly conserved toxin produced by GBS capable of disrupting epithelial barriers. However, its role in the pathogenesis of late-onset GBS disease is unknown. Our aim was to determine the contribution of βH/C to intestinal colonization and translocation to extraintestinal tissues. Using our established mouse model of late-onset GBS disease, we exposed animals to GBS COH-1 (WT), a βH/C-deficient mutant (KO), or vehicle control (PBS) via gavage. Blood, spleen, brain, and intestines were harvested 4 days post-exposure for determination of bacterial burden and isolation of intestinal epithelial cells. We used RNA-sequencing to examine the transcriptomes and performed gene ontology enrichment and KEGG pathway analysis. A separate cohort of animals were followed longitudinally to compare colonization kinetics and mortality between WT and KO groups. We demonstrate that disseminated to extraintestinal tissues occurred only in the WT exposed animals. We observed major transcriptomic changes in the colon of colonized animals, but not in the small intestine. We noted differential expression of genes among WT and KO exposed mice indicating that βH/C contributes to alterations in epithelial barrier structure and immune response signaling. Overall, our results demonstrate an important role for βH/C in the pathogenesis of late-onset GBS disease.

2023-05-31 | GSE230856 | GEO

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