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Unknown,Transcriptomics,Genomics,Proteomics

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Intralesional host response within eschars in Mediterranean spotted fever

ABSTRACT: The host response within the eschar of inoculation during Mediterranean spotted fever (MSF) has been poorly studied. Our objective was to evaluate the host response by comparing transcriptional profiles of eschars to controls using a whole-genome microarray. Hierarchical clustering revealed a signature of eschars consisting of 698 genes. The genes included in this signature were mainly up-regulated and were predominantly associated with immune response and signalling. New molecules involved notably in microbicidal and innate immunity response have also been found up-regulated in eschars such as MMP1, Defensin β4, the proinflammatory S100A9, and the T cell attracting CCL-18. Genes down-regulated were mainly associated with biological regulation. We also observed that eschars from severe cases of MSF displayed a specific signature with notably difference in degree of modulation compared to eschars from non severe MSF cases. Some parameters identified in this work should be tested as biomarkers for prognostic assessment in future studies. To evaluate the host response by comparing transcriptional profiles of eschars to controls

ORGANISM(S): Homo sapiens

SUBMITTER: adil ef

PROVIDER: E-GEOD-32993 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Intralesional host response within eschars in Mediterranean spotted fever

Project description:The host response within the eschar of inoculation during Mediterranean spotted fever (MSF) has been poorly studied. Our objective was to evaluate the host response by comparing transcriptional profiles of eschars to controls using a whole-genome microarray. Hierarchical clustering revealed a signature of eschars consisting of 698 genes. The genes included in this signature were mainly up-regulated and were predominantly associated with immune response and signalling. New molecules involved notably in microbicidal and innate immunity response have also been found up-regulated in eschars such as MMP1, Defensin β4, the proinflammatory S100A9, and the T cell attracting CCL-18. Genes down-regulated were mainly associated with biological regulation. We also observed that eschars from severe cases of MSF displayed a specific signature with notably difference in degree of modulation compared to eschars from non severe MSF cases. Some parameters identified in this work should be tested as biomarkers for prognostic assessment in future studies.

2012-12-07 | GSE32993 | GEO

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Project description:Papillary thyroid cancer (PTC) accounts for the predominant histological types of all thyroid cancers. Additionally, 15% PTC with LNM are unfortunately associated with increased radioiodine resistance, distant metastasis, recurrence and increased mortality. Additionally, 15% PTC with LNM are unfortunately associated with increased radioiodine resistance, distant metastasis, recurrence and increased mortality.Two proteomics research has been implemented to investigate the molecular mechanisms involved in pathogenesis of PTC patients younger than 45 years with LNM and identified several candidate biomarker.However, until now there is no study to comprehensively investigate the differential expressed proteins (DEPs) in PTC patients older than age 45 years.

2022-06-09 | PXD007971 | Pride

Sublytic concentrations of Staphylococcus aureus Panton-Valentine leukocidin alter human polymorphonuclear leukocyte gene expression and enhance bactericidal capacity.

Project description:Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) infections are often caused by strains encoding Panton-Valentine leukocidin (PVL). PVL can cause lysis of polymorphonuclear leukocytes (PMNs) and other myeloid cells in vitro, a function considered widely as the primary means by which PVL might contribute to disease. However, at sublytic concentrations PVL can function as a PMN agonist. To better understand this phenomenon, we investigated the ability of PVL to alter human PMN function. PMNs exposed to PVL had enhanced capacity to produce superoxide in response to N-formyl-methionyl-leucyl-phenylalanine (fMLF), but unlike priming by lipopolysaccharide, this response did not require Toll-like receptor signal transduction. On the other hand, there was subcellular redistribution of NADPH oxidase components in PMNs following exposure of these cells to PVL - a finding consistent with priming. Priming of PMNs with other agonists such as IL-8 or GM-CSF altered the ability PVL to cause formation of pores in the plasma membranes of these cells. Microarray analysis revealed significant changes in the human PMN transcriptome following exposure to PVL, including up-regulation of molecules that regulate the inflammatory response. Consistent with the microarray data, mediators of the inflammatory response were released from PMNs after stimulation with PVL. We conclude that exposure of human PMNs to sublytic concentrations of PVL elicits a proinflammatory response that is regulated in part at the level of gene expression. We propose that PVL-mediated priming of PMNs enhances the host innate immune response. time series of PMN's non treated vs PVL treated vs iPVL treated

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2023-11-30 | E-MTAB-13563 | biostudies-arrayexpress

DNA-seq or genomic RNA region of HIV-1 reverse transcriptase, protease and integrase gene

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2014-09-04 | E-MEXP-3684 | biostudies-arrayexpress

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Project description:MSF-NIGER

| PRJEB50347 | ENA

Serum Proteomics of Severe Fever with Thrombocytopenia Syndrome Patients

Project description:Dabie bandavirus, also termed as severe fever with thrombocytopenia syndrome virus (SFTSV), was first isolated in China in 2010. At this time, the virus was found to have spread to South Korea, Japan, and other countries. A high case fatality rate is reported for SFTS, ranging from 12–50% within various sources. Several omics for clinical studies among SFTS patients as well as studies of cultured SFTSV have attempted to characterize the relevant molecular biology and epidemiology of the disease. However, a global serum proteomics analysis among SFTS patients has not yet been reported to date. Thrombocytopenia and multiple organ failure are the major immediate causes of death among SFTS patients. In this study, serum proteomic changes related to thrombocytopenia, abnormal immune response, and inflammatory activation were documented in SFTS patients. These findings provide useful information forunderstanding the clinical manifestations of SFTS.

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