Transcription profiling of human T Cell and monocyte populations, leukocyte or leukocyte subpopulations and skeletal muscle
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: IDDC Inflammation the Host Response to Injury
PROVIDER: E-GEOD-2328 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Application of genome-wide expression analysis to human health and disease.
Cobb J Perren JP Mindrinos Michael N MN Miller-Graziano Carol C Calvano Steve E SE Baker Henry V HV Xiao Wenzhong W Laudanski Krzysztof K Brownstein Bernard H BH Elson Constance M CM Hayden Douglas L DL Herndon David N DN Lowry Stephen F SF Maier Ronald V RV Schoenfeld David A DA Moldawer Lyle L LL Davis Ronald W RW Tompkins Ronald G RG Baker Henry V HV Bankey Paul P Billiar Timothy T Brownstein Bernard H BH Calvano Steve E SE Camp David D Chaudry Irshad I Cobb J Perren JP Davis Ronald W RW Elson Constance M CM Freeman Bradley B Gamelli Richard R Gibran Nicole N Harbrecht Brian B Hayden Douglas L DL Heagy Wyrta W Heimbach David D Herndon David N DN Horton Jureta J Hunt John J Laudanski Krzysztof K Lederer James J Lowry Stephen F SF Maier Ronald V RV Mannick John J McKinley Bruce B Miller-Graziano Carol C Mindrinos Michael N MN Minei Joseph J Moldawer Lyle L LL Moore Ernest E Moore Frederick F Munford Robert R Nathens Avery A O'keefe Grant G Purdue Gary G Rahme Laurence L Remick Daniel D Sailors Matthew M Schoenfeld David A DA Shapiro Michael M Silver Geoffrey G Smith Richard R Stephanopoulos Gregory G Stormo Gary G Tompkins Ronald G RG Toner Mehmet M Warren Shaw S West Michael M Wolfe Steven S Xiao Wenzhong W Young Vernon V
Proceedings of the National Academy of Sciences of the United States of America 20050321 13
The application of genome-wide expression analysis to a large-scale, multicentered program in critically ill patients poses a number of theoretical and technical challenges. We describe here an analytical and organizational approach to a systematic evaluation of the variance associated with genome-wide expression analysis specifically tailored to study human disease. We analyzed sources of variance in genome-wide expression analyses performed with commercial oligonucleotide arrays. In addition, ...[more]
Similar Datasets
Project description:expression files supporting: Application of genome-wide expression analysis to human health and disease. PNAS Supplementary Information: http://www.gluegrant.org/pubsupport/PNAS_1/ Keywords = clinical studies Keywords = gene expression Keywords = inflammation Keywords = microarray Keywords = trauma Keywords: other
2005-02-24 | GSE2328 | GEO
Project description:Major efforts are invested in the analysis of phenotypic variation in a population of individuals. While many of these studies focus on the genetic basis of phenotypic variation via measurements of DNA polymorphic sites, the environmental effects are still elusive. Here we propose a methodology, called CCCE ('Cell Composition Common Environment'), to identify environmental effects on the composition of immune cell functionalities. Specifically, CCCE is focused on the common experiences that are shared between siblings (the 'common environment'), designed to correct for cell subpopulation heterogeneity, and is based on a multicolor flow cytometry analysis across a large cohort of human monozygotic and dizygotic twins. We demonstrate that the CCCE methodology can provide insights on the relations between common environmental effects and the heterogenic functions of several immune cell types, such as NK cells effector functions and coagulation-related capabilities of monocytes. The software described in this article is available at http://csgi.tau.ac.il/CCCE.
| S-EPMC5915319 | biostudies-literature
Project description:BACKGROUND:Neonate immune cell functions lack full protection against pathogens. This could be either defect or protective mechanism against overshooting proinflammatory immune responses. We here analysed the function of classical, pro- and anti-inflammatory monocytes and granulocytes from neonates in comparison with adults to investigate if suppressed functions of subpopulations are causative for the unique neonatal immune status. Therefore, reactive oxygen species (ROS) and surface activation markers were quantified in subpopulations. METHODS:In a prospective, longitudinal study granulocyte and monocyte subpopulations were analysed in healthy term infants (>?37?week; n =?13) in comparison with healthy young adults (n =?11). Percentage (%) of cells expressing surface marker (HLA-DR, CD11b, CD62L, CD32, Toll-Like-Receptor-2) and expression per cell, determined by mean fluorescence intensity (MFI), were measured by flow cytometry. ROS production was induced by fMLP, PMA and E. coli in term neonates (>?37?week; n =?13). RESULTS:Classical granulocytes were down- and proinflammatory granulocytes upregulated in neonates compared with adults. Percentage of TLR-2 expressing granulocytes was increased in neonates. Granulocytic ROS production depended on stimulation. The percentage of anti-inflammatory monocytes was increased, while classical monocytes were reduced in neonates. HLA-DR (%, MFI) showed reduction for all monocyte subpopulations, while CD32, CD11b, CD62L and TLR-2 were differently regulated in comparison with adults. CONCLUSIONS:Differentially regulated granulocyte and monocyte subpopulations indicate a unique state of neonatal immunity to fight infections and prevent dysregulation. Further studies are needed to investigate the role of reduced granulocytic ROS formation and reduced monocytic HLA-DR in active disease.
| S-EPMC6884604 | biostudies-literature
Project description:CD44 expressed in monocytes and lymphocytes seems to play a crucial role in gastrointestinal inflammation, such as the one occurring in the context of inflammatory bowel diseases. Differentially methylated genes are distinctly expressed across monocyte subpopulations related to the state of Crohn's disease. Hence, the aim of this study was to detect CD44 expression in leukocyte subpopulations in relation to the type of IBD, therapy, and disease duration. Monocyte subpopulations CD14++CD16-, CD14++CD16++, and CD14+CD16+ as well as other leukocytes were analyzed for their CD44 expression using flow cytometry in 46 patients with IBD and 48 healthy controls. Patients with Crohn's disease treated with non-biological therapy (NBT) exhibited a lower percentage of anti-inflammatory CD14+CD16++ monocytes, whereas NBT-treated patients with ulcerative colitis had lower expression of CD44 on CD14+CD44+ lymphocytes in comparison to controls, respectively. Conversely, patients with Crohn's disease treated with biological therapy had a higher percentage of CD44+ granulocytes but lower expression of CD44 on anti-inflammatory monocytes compared to controls. Median fluorescence intensity (MFI) of CD44 on CD44+CD14+ lymphocytes was higher in ulcerative colitis patients treated with biological therapy compared to NBT. The percentage of classical CD14++CD16- monocytes was lower in the <9 years of IBD duration subgroup compared with the longer disease duration subgroup. The present study addresses the putative role of differentiation and regulation of leukocytes in tailoring IBD therapeutic regimes.
| S-EPMC9407096 | biostudies-literature
Project description:In the intestine, epithelial factors condition incoming immune cells including monocytes to adapt their threshold of activation and prevent undesired inflammation. Colonic epithelial cells express Secretory Leukocyte Protease Inhibitor (SLPI), an inhibitor of NF kappa light chain enhancer of activated B cells (NF-κB) that mediates epithelial hyporesponsiveness to microbial stimuli. Uptake of extracellular SLPI by monocytes has been proposed to inhibit monocyte activation. We questioned whether monocytes can produce SLPI and whether endogenous SLPI can inhibit monocyte activation. We demonstrate that human THP-1 monocytic cells produce SLPI and that CD68+ SLPI-producing cells can be detected in human intestinal lamina propria. Knockdown of SLPI in human THP-1 cells significantly increased NF-κB activation and subsequent C-X-C motif chemokine ligand 8 (CXCL8) and TNF-α production in response to microbial stimulation. Reconstitution of SLPI-deficient cells with either full-length SLPI or SLPI lacking its signal peptide rescued inhibition of NF-κB activation and cytokine production, demonstrating that endogenous SLPI inhibits monocytic cell activation. Unexpectedly, exogenous SLPI did not inhibit CXCL8 or TNF-α production, despite efficient uptake. Our data argue that endogenous SLPI can regulate the threshold of activation in monocytes, thereby preventing activation by commensal bacteria in mucosal tissues.
| S-EPMC10107746 | biostudies-literature
Project description:The progressive accumulation of monocyte-derived cells in the atherosclerotic plaque is a hallmark of atherosclerosis. However, it is now appreciated that monocytes represent a heterogeneous circulating population of cells that differ in functionality. New approaches are needed to investigate the role of monocyte subpopulations in atherosclerosis since a detailed understanding of their differential mobilization, recruitment, survival and emigration during atherogenesis is of particular importance for development of successful therapeutic strategies. We present a novel methodology for the in vivo examination of monocyte subpopulations in mouse models of atherosclerosis. This approach combines cellular labeling by fluorescent beads with multiphoton microscopy to visualize and monitor monocyte subpopulations in living animals. First, we show that multiphoton microscopy is an accurate and timesaving technique to analyze monocyte subpopulation trafficking and localization in plaques in excised tissues. Next, we demonstrate that multiphoton microscopy can be used to monitor monocyte subpopulation trafficking in atherosclerotic plaques in living animals. This novel methodology should have broad applications and facilitate new insights into the pathogenesis of atherosclerosis and other inflammatory diseases.
| S-EPMC3443108 | biostudies-literature
Project description:In vivo studies in mice have identified subsets of monocytes involved in the inflammatory response to pathogens, but their respective functions remains poorly understood. We report that human CD14+ monocytes represent functional ortholog to mouse Ly6C+ monocytes and are responsible for phagocytosis, Reactive Oxygen Species (ROS) and cytokine production in response to a broad range of pathogen associated molecular patterns (PAMP). In contrast a discrete population of CD14dim cells are ortholog to the mouse ly6C- monocytes and share their ability to patrol the endothelium of blood vessels, but do not produce ROS, are weak phagocytes, and poorly respond to bacterial PAMPs. Instead, CD14dim monocytes are critical for production of pro-apoptotic and pro-inflammatory cytokines in response to viruses and nucleic acids via a unique TLR7-8/MyD88/MEK pathway, while they may also contribute to tissue damage in autoimmune diseases such as Lupus.
2011-01-07 | E-MEXP-2544 | biostudies-arrayexpress
Project description:Spondyloarthropathies (SpA) are a family of rheumatic disorders that could be divided into axial (axSpA) and peripheral (perSpA) sub-forms depending on the disease clinical presentation. The chronic inflammation is believed to be driven by innate immune cells such as monocytes, rather than self-reactive cells of adaptive immune system. The aim of the study was to investigate the micro-RNA (miRNA) profiles in monocyte subpopulations (classical, intermediate and non-classical subpopulations) acquired from SpA patients or healthy individuals in search for prospective disease specific and/or disease subtype differentiating miRNA markers. Several SpA-specific and axSpA/perSpA differentiating miRNAs have been identified that appear to be characteristic for specific monocyte subpopulation. For classical monocytes, upregulation of miR-567 and miR-943 was found to be SpA-specific, whereas downregulation of miR-1262 could serve as axSpA-differentiating, and the expression pattern of miR-23a, miR-34c, mi-591 and miR-630 as perSpA-differentiating markers. For intermediate monocytes, expression levels of miR-103, miR-125b, miR-140, miR-374, miR-376c and miR-1249 could be used to distinguish SpA patients from healthy donors, whereas the expression pattern of miR-155 was identified as characteristic for perSpA. For non-classical monocytes, differential expression of miR-195 was recognized as general SpA indicator, while upregulation of miR-454 and miR-487b could serve as axSpA-differentiating, and miR-1291 as perSpA-differentiating markers. Our data indicate for the first time that in different SpA subtypes, monocyte subpopulations bear disease-specific miRNA signatures that could be relevant for SpA diagnosis/differentiation process and may help to understand SpA etiopathology in the context of already known functions of monocyte subpopulations.
| S-EPMC10149963 | biostudies-literature
Project description:Prenatal arsenic exposure is associated with increased risk of disease in adulthood. This has led to considerable interest in arsenic's ability to disrupt fetal programming. Many studies report that arsenic exposure alters DNA methylation in whole blood but these studies did not adjust for cell mixture. In this study, we examined the relationship between arsenic in maternal drinking water collected ≤ 16 weeks gestational age and DNA methylation in cord blood (n = 44) adjusting for leukocyte-tagged differentially methylated regions. DNA methylation was quantified using the Infinium HumanMethylation 450 BeadChip array. Recursively partitioned mixture modeling examined the relationship between arsenic and methylation at 473,844 CpG sites. Median arsenic concentration in water was 12 µg/L (range<1- 510 µg/L). Log 10 arsenic was associated with altered DNA methylation across the epigenome (P = 0.002); however, adjusting for leukocyte distributions attenuated this association (P = 0.013). We also observed that arsenic had a strong effect on the distribution of leukocytes in cord blood. In adjusted models, every log 10 increase in maternal drinking water arsenic exposure was estimated to increase CD8+ T cells by 7.4% (P = 0.0004) and decrease in CD4+ T cells by 9.2% (P = 0.0002). These results show that prenatal exposure to arsenic had an exposure-dependent effect on specific T cell subpopulations in cord blood and altered DNA methylation in cord blood. Future research is needed to determine if these small changes in DNA methylation alter gene expression or are associated with adverse health effects.
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Project description:The aim of this study was to identify cell-type specific contributions to the acute HIV transcriptional signature identified in the CHAVI 001 acute 32 prospective cohort.
2016-02-15 | GSE25669 | GEO