Ontology highlight
ABSTRACT:
PROVIDER: PRJNA837225 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Patients were recruited at the Hospital do Cancer AC Camargo (São Paulo/Brazil), Instituto de Enfermedades Neoplasicas - INEN (Lima, Peru), Hospital Araujo Jorge (Goiania, Brazil) and Hospital Heliopolis (São Paulo, Brazil).All patients signed a pre-informed consent and the study was approved by the internal ethics committee. Tissue samples were snap frozen in liquid nitrogen . Before RNA extraction histopathological diagnosis was re-confirmed, all samples were micro-dissected and only tissues with at least 70% of tumor cells and no visible infiltrating inflammatory cells were used as tumor. Morphologically disease-free tissue obtained from surgical margins was considered as normal. A total of 38 samples were analyzed: 8 normal tissues, 10 goiters, 10 adenomas and 10 papillary carcinomas. Keywords: other
2005-05-09 | GSE2468 | GEO
Project description:Patients were recruited at the Hospital do Cancer AC Camargo (São Paulo/Brazil), Instituto de Enfermedades Neoplasicas - INEN (Lima, Peru), Hospital Araujo Jorge (Goiania, Brazil) and Hospital Heliopolis (São Paulo, Brazil).All patients signed a pre-informed consent and the study was approved by the internal ethics committee. Tissue samples were snap frozen in liquid nitrogen . Before RNA extraction histopathological diagnosis was re-confirmed, all samples were micro-dissected and only tissues with at least 70% of tumor cells and no visible infiltrating inflammatory cells were used as tumor. Morphologically disease-free tissue obtained from surgical margins was considered as normal. A total of 38 samples were analyzed: 8 normal tissues, 10 goiters, 10 adenomas and 10 papillary carcinomas. Keywords: other
2010-06-10 | E-GEOD-2468 | biostudies-arrayexpress
Project description:D. vulgaris is a model sulfate reducing bacteria whose genome encodes a high number of two component systems, including 29 DNA-binding response regulators (RRs) whose functions are unknown, but are very likley to be important to the environmental lifestyle of the organism. We determined the gene targets for 24 of these RRs using purified His-tagged RR and sheared genomic DNA in an in vitro DAP-chip (DNA-affinity-purified - chip) assay. For each RR, one target was identified first using gel shift assays, and qPCR was used to ensure that the target was enriched in the RR-bound DNA before the samples were hybridized to a tiling array. Based on the peaks generated by the array analysis, we determined that at least 200 genes are regulated by two component systems in this organism. We also predicted binding site motifs and validated them for 15 RRs using gel shift assays.
2011-05-31 | GSE25163 | GEO
Project description:Reversal reactions (RR) in leprosy provide a unique opportunity to study the dynamics of the immune response against intracellular bacteria in humans. We performed RNA sequencing on paired skin biopsy specimens from nine leprosy patients before and during RR, identifying a 64-gene antimicrobial response signature that correlated with the concomitant decrease in Mycobacterium leprae bacilli in RR patients. The upstream regulators of this antimicrobial gene signature included both innate (IL-1β, TNF) and adaptive (IFN-γ, IL-17) cytokines, indicating induction of both Th1 and Th17 responses. By using a machine learning classifier to identify proteins with predicted membrane-permeating activity, we identified 28 additional antimicrobial genes including S100A8. We validated the antimicrobial activity of four proteins (S100A7, S100A8, CCL17, CCL19) against M. leprae in infected macrophages and axenic culture. Scanning electron microscopy revealed distinct morphological changes in bacterial membranes upon exposure to these antimicrobial proteins. Our findings illuminate the dynamic regulation of antimicrobial gene expression as part of the innate and adaptive immune response against M. leprae and identify new potential antimicrobial effectors in human host defense. These insights underscore the potential for therapeutic strategies aimed at enhancing Th1 and Th17 cell function to improve outcomes in mycobacterial infection in humans.
2024-12-21 | GSE280021 | GEO
Project description:The ability to respond to stress is at the core of an organismâs survival. The hormones epinephrine and norepinephrine play a central role in stress responses in mammals, which require the synchronized interaction of the whole neuroendocrine system. Bacteria also sense and respond to epinephrine and norepinephrine as a means to gauge the metabolic and immune state of the host. Mammalian adrenergic receptors are G-coupled protein receptors (GPCRs), bacteria, however, sense these hormones through histidine sensor kinases (HKs). HKs autophosphorylate in response to multiple signals and transfer this phosphate to response regulators (RRs). Two bacterial adrenergic receptors have been identified in EHEC, QseC and QseE, with QseE being downstream of QseC in this signaling cascade. We mapped the QseC signaling cascade in the deadly pathogen enterohemorrhagic E. coli (EHEC), which exploits this signaling system to promote disease. Through QseC, EHEC activates expression of metabolic, virulence and stress response genes, synchronizing the cell response to these stress hormones. Coordination of these responses is achieved by QseC phosphorylating three of the thirty two EHEC RRs. The QseB RR, which is QseCâs cognate RR, activates the flagella regulon which controls bacteria motility and chemotaxis. The QseF RR, which is phosphorylated by the QseE adrenergic sensor, coordinates expression of virulence genes involved in formation of lesions in the intestinal epithelia by EHEC, and the bacterial SOS stress response. The third RR, KdpE, controls potassium uptake, osmolarity response, and also the formation of lesions in the intestine. Adrenergic regulation of bacterial gene expression shares several parallels with mammalian adrenergic signaling having profound effects in the whole organism. Understanding adrenergic regulation of a bacterial cell is a powerful approach to study the underlying mechanisms of stress and cellular survival. Experiment Overall Design: Microarray comparisons reveal some trends with respect to signaling cascades. Comparative methods were used to identify networks.
2009-11-16 | E-GEOD-15050 | biostudies-arrayexpress
Project description:D. vulgaris is a model sulfate reducing bacteria whose genome encodes a high number of two component systems, including 29 DNA-binding response regulators (RRs) whose functions are unknown, but are very likley to be important to the environmental lifestyle of the organism. We determined the gene targets for 24 of these RRs using purified His-tagged RR and sheared genomic DNA in an in vitro DAP-chip (DNA-affinity-purified - chip) assay. For each RR, one target was identified first using gel shift assays, and qPCR was used to ensure that the target was enriched in the RR-bound DNA before the samples were hybridized to a tiling array. Based on the peaks generated by the array analysis, we determined that at least 200 genes are regulated by two component systems in this organism. We also predicted binding site motifs and validated them for 15 RRs using gel shift assays. In vitro DAP-chip for 28 response regulators where RR-bound enriched DNA is compared to input total genomic DNA
2011-05-31 | E-GEOD-25163 | biostudies-arrayexpress
Project description:The ability to respond to stress is at the core of an organism’s survival. The hormones epinephrine and norepinephrine play a central role in stress responses in mammals, which require the synchronized interaction of the whole neuroendocrine system. Bacteria also sense and respond to epinephrine and norepinephrine as a means to gauge the metabolic and immune state of the host. Mammalian adrenergic receptors are G-coupled protein receptors (GPCRs), bacteria, however, sense these hormones through histidine sensor kinases (HKs). HKs autophosphorylate in response to multiple signals and transfer this phosphate to response regulators (RRs). Two bacterial adrenergic receptors have been identified in EHEC, QseC and QseE, with QseE being downstream of QseC in this signaling cascade. We mapped the QseC signaling cascade in the deadly pathogen enterohemorrhagic E. coli (EHEC), which exploits this signaling system to promote disease. Through QseC, EHEC activates expression of metabolic, virulence and stress response genes, synchronizing the cell response to these stress hormones. Coordination of these responses is achieved by QseC phosphorylating three of the thirty two EHEC RRs. The QseB RR, which is QseC’s cognate RR, activates the flagella regulon which controls bacteria motility and chemotaxis. The QseF RR, which is phosphorylated by the QseE adrenergic sensor, coordinates expression of virulence genes involved in formation of lesions in the intestinal epithelia by EHEC, and the bacterial SOS stress response. The third RR, KdpE, controls potassium uptake, osmolarity response, and also the formation of lesions in the intestine. Adrenergic regulation of bacterial gene expression shares several parallels with mammalian adrenergic signaling having profound effects in the whole organism. Understanding adrenergic regulation of a bacterial cell is a powerful approach to study the underlying mechanisms of stress and cellular survival.
2009-09-15 | GSE15050 | GEO
Project description:Gene expression data from whole-blood collected from Kenyan children with Plasmodium falciparum malaria infection at acute hospital admission (n=15) and at convalescence (n=9). A clinical history design type is where the organisms clinical history of diagnosis, treatments, e.g. vaccinations, surgery etc. Disease State: with Plasmodium falciparum malaria infection at acute hospital admission and at convalescence
2016-02-15 | GSE35860 | GEO
Project description:Opioids analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit their use. It has been recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. Further study indicated distinct alterations in the gut microbiome and metabolome following morphine treatment, contributing to the negative consequences associated with opioid use. However, it is unclear how opioids modulate gut homeostasis in the context of a hospital acquired bacterial infection. In the current study, a mouse model of C. rodentium infection was used to investigate the role of morphine in the modulation of gut homeostasis in the context of a hospital acquired bacterial infection. Citrobacter rodentium is a natural mouse pathogen that models intestinal infection by enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) and causes attaching and effacing lesions and colonic hyperplasia. Morphine treatment resulted in 1) the promotion of C. rodentium systemic dissemination, 2) increase in virulence factors expression with C. rodentium colonization in intestinal contents, 3) altered gut microbiome, 4) damaged integrity of gut epithelial barrier function, 5) inhibition of C. rodentium-induced increase in goblet cells, and 6) dysregulated IL-17A immune response. This is the first study to demonstrate that morphine promotes pathogen dissemination in the context of intestinal C. rodentium infection, indicating morphine modulates virulence factor-mediated adhesion of pathogenic bacteria and induces disruption of mucosal host defense during C. rodentium intestinal infection in mice. This study demonstrates and further validates a positive correlation between opioid drug use/abuse and increased risk of infections, suggesting over-prescription of opioids may increase the risk in the emergence of pathogenic strains and should be used cautiously. Therapeutics directed at maintaining gut homeostasis during opioid use may reduce the comorbidities associated with opioid use for pain management.
2020-02-18 | E-MTAB-7503 | biostudies-arrayexpress