Human PBMNCs: Control vs. Patients with Kawasaki disease
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE17975 | GEO | 2010/09/04
SECONDARY ACCESSION(S): PRJNA120001
REPOSITORIES: GEO
Similar Datasets
Project description:Genes that were consistently up-regulated in KD patients compared with healthy controls, and that showed over 2.0 or 3.0-fold differences by the comparison between the two groups in the mean expression levels were selected. Microarray analysis for PBMNCs of acute-phase KD patients was performed using an AceGene Human Oligo Chip 30K 1 Chip Version (Hitachi Software Engineering) that contains approximately 30,000 genes. In the study presented here, 3 cases of Kawasaki disease at acute phase,and 5 healthy controls,were used. The data with low signal-to-noise ratios (S/N<3) were not used for further analysis.
2010-09-04 | E-GEOD-17975 | biostudies-arrayexpress
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2020-11-30 | GSE149333 | GEO
Project description:We compared the abundance of gene transcripts of whole blood RNA between IVIG-resistant and –responsive KD patients to identify biomarkers that might differentiate between these two groups and to generate new targets for therapies in IVIG-resistant KD patients.
2009-10-17 | GSE18606 | GEO
Project description:Background: Kawasaki disease (KD) is a multisystemic vasculitis of unknown aetiology in children. KD with coronary artery lesion is now the leading acquired heart disease in children. Peripheral blood mononuclear cells (PBMCs) play roles in KD. We identified hub genes based on RNA sequencing data and validated them in PBMCs and human umbilical vein endothelial cells (HUVECs) coculture with PBMCs. Methods: mRNA microarray of PBMCs from 12 acute KD patients and 12 healthy controls was performed to screen differentially expressed mRNAs (DE-mRNAs). We selected 20 KD patients and 20 healthy controls for validation, and established HUVECs coculture with PBMCs. Real time-PCR was finally conducted to confirm the reliability and validity of the expression level of DE-mRNAs from PBMCs and HUVECs coculture. Results: A total of 6039 DE-mRNAs were found (2267 upregulated, 3772 downregulated). Thirty hub genes were selected. KD PBMCs significantly impaired HUVECs viability and migration. IL1R2 was downregulated, FCGR1A, and CD177 mRNAs were upregulated in acute KD. IL1R2 was elevated, FCGR1A and CD177 mRNAs were downregulated in convalescence. And the real-time PCR and ELISA results showed IL1R2 was downregulated in acute KD PBMC-HUVECs co-cultures and elevated in convalescence. Conclusion: These findings may improve our understanding of PBMCs and HUVECs coculture with PBMCs in KD.
2026-03-26 | GSE325833 | GEO
Project description:Kawasaki disease (KD) is considered the main contributor to acquired heart diseases in developed countries. However, the precise pathogenesis of KD remains unclear. Neutrophils played roles in KD. This study aimed to select hub genes in neutrophils in acute KD. mRNA microarray of neutrophils from four acute KD patients and three healthy controls was performed to screen differentially expressed mRNAs (DE-mRNAs). DE-mRNAs were analyzed and predicted by Gene Ontology (GO), Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathways, and protein-protein interaction networks. Real time-PCR was finally conducted to confirm the reliability and validity of the expression level of DE-mRNAs from blood samples of healthy controls and KD patients in both acute and convalescent stage.
2023-02-20 | GSE222215 | GEO
Project description:Infliximab (IFX) has been reported as the further therapy in intravenous immunoglobulin G (IVIG)-resistant Kawasaki disease (KD) patients. IFX is a monoclonal antibody that blocks the pro-inflammatory cytokine tumor necrosis factor (TNF)-α, but how IFX affect KD vasculitis is unknown. We investigated expression profiling of whole blood cells to elucidate the molecular mechanisms of the effectiveness of IFX therapy and to find characteristic biomarker and an important target in refractory KD. Methods: Refractory KD patients who failed to respond to repeated intravenous immunoglobulin G (IVIG) infusions had received a single infusion of IFX as third therapy. To validate specifically transcripts abundance for IFX therapy, we detected the altered transcripts expression and signaling pathways of whole blood mRNA in these IFX-responsive patients (n=8) using Affymetrix array, comparing initial IVIG-responsive patients (n=6).Results: A total of 1,388 transcripts abundance were significantly altered before and after IFX treatment. These transcripts abundance in IFX had Nucleotide-binding oligomerization domain pathway that play a role in activation of NFκB and IL-1 signaling pathway outside the field of TNF-α signaling pathway. Fifty transcripts including Peptidase inhibitor-3 (PI3), Matrix metalloproteinase-8 (MMP8), Chemokine (C-C motif) receptor-2 (CCR2) and Pentraxin-3 (PTX3) were significantly down-regulated in IFX. Conclusion: We demonstrated that the inhibition of TNF-α by IFX have affected various molecular mechanism materially for IVIG-resistant KD patients. 28 samples of pre- and post-treatment in IFX-responsive patients (n=8) and IVIG-responsive patients (n=6).
2014-04-30 | E-GEOD-48498 | biostudies-arrayexpress
Project description:The diagnosis of Kawasaki disease (KD) is often difficult to distinguish from adenovirus (HAdV) and Group A streptococcal disease (GAS). We sought to: 1) to define the KD transcriptional signature that can aid in the diagnosis of complete and incomplete KD in children; 2) to identify specific biomarkers that objectively discriminate between KD and other mimicking conditions, including HAdV and 3) to test the prognostic utility of GEP to determine response to IVIG therapy and development of coronary artery lesions (CAL). Methods: Blood RNA samples were analyzed from 76 pediatric patients with complete KD, 13 with incomplete KD, 19 patients with HAdV, 17 patients with GAS disease, and age- and sex-matched healthy controls (HC). We used class comparisons (MW p< 0.01, Benjamini-Hochberg, and 1.25 fold change filter), class prediction, modular analysis and MDTH analyses to define the specificity of the KD profiles and identify markers of severity. Results: Statistical group comparisons identified 7,899 genes differentially expressed in 39 complete KD patients versus HC (KD biosignature). This signature was validated in another 37 patients with complete KD and in 13 patients with incomplete KD. Modular analysis in children with complete KD demonstrated overexpression of inflammation, neutrophils, myeloid cell, coagulation cascade, and cell cycle genes. The KNN class prediction algorithm identified 25-classifier genes that differentiated children with KD vs HAdV infection in two independent cohorts of patients with 96% (95% CI [80%-99%]) sensitivity and 95% [74%-99%] specificity. MDTH scores in KD patients significantly correlated with the baseline c-reactive protein (R=0.29, p=0.008) and was four fold higher than in children with HAdV (p<0.01). In addition, KD patients that remained febrile 36 hours after treatment with IVIG (non-responders) demonstrated higher baseline, pre-treatment MDTH values compared with responders [12,290 vs. 5,572 respectively; p=0.009]. Conclusion: Transcriptional signatures can be used as a tool to discriminate between KD and HAdV infection, and may also provide prognostic information. 113 samples, no replicates, 9 HAdV, 57 cKD, 12 FUO, 13 GAS, 3 GAS/SF, 5 inKD, 14 healthy control
2016-04-14 | E-GEOD-68004 | biostudies-arrayexpress
Project description:Abstract: Although Kawasaki disease (KD) and Multisystem inflammatory syndrome in children (MIS-C) share some clinical manifestations, their cardiovascular outcomes are different, and this may be reflected at the level of the endothelial cell (EC). We performed RNA-seq on cultured ECs incubated with pre-treatment sera from KD (n=5), MIS-C (n=7), and healthy controls (n=3). We conducted Weighted Gene Co-expression Network Analysis (WGCNA) using 935 transcripts differentially expressed between MIS-C and KD using soft filtering (un-adjusted p<0.05, >1.1 fold difference). We found seven gene modules annotated as increased TNFα/NFB pathway, decreased Endothelial-Mesenchymal Transition (EndoMT) and EC homeostasis, an-ti-inflammation and immune response, translation, and glucocorticoid responsive gene suppression in MIS-C. To further understand the difference in the EC response between KD and MIS-C, a hard filter was applied to identify 41 differentially expressed genes (DEGs) between KD and MIS-C (adjusted p<0.05, >2 fold-difference). Again, the majority was NFB pathway genes including nine upregulated pro-survival genes. Expression levels were higher in the genes influencing autophagy (UBD, EBI3, and SQSTM1). Other DEGs also supported the finding by WGCNA. Compared to KD, ECs in MIS-C had increased pro-survival transcripts, but reduced transcripts related to EndoMT and EC homeostasis. These differences in EC response may in-fluence the different cardiovascular outcomes in these two diseases.
2023-08-21 | GSE236833 | GEO
Project description:ABSTRACT Background. Acute Kawasaki disease (KD) is difficult to distinguish from other acute rash/fever illnesses, in part because the etiologic agent(s) and pathophysiology remain poorly characterized. As a result, diagnosis and critical therapies may be delayed. Methods. We used DNA microarrays to identify possible diagnostic features of KD. We compared gene expression patterns in the blood of 23 children with acute KD and 18 age-matched febrile children with three illnesses that resemble KD. Results. Genes associated with platelet and neutrophil activation were expressed at higher levels in KD patients than in patients with acute adenovirus infections or systemic adverse drug reactions but not in patients with scarlet fever; genes associated with B cell activation were also expressed at higher levels in KD patients than in controls. A striking absence of interferon-stimulated gene expression in the KD patients was confirmed in an independent cohort of KD subjects. We successfully predicted the diagnosis in 21 of 23 KD patients and 7 of 8 adenovirus patients using a set of 38 gene transcripts. Conclusions. These findings provide insight into the molecular features that distinguish KD from other febrile illnesses, and support the feasibility of developing novel diagnostic reagents for KD based on the host response. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Disease State: One of Kawasaki Disease (KD) or control (C) of Scarlet fever (C-sf), adenovirus infection (C-ai) or drug reaction (C-dr) disease_state_design
2010-06-24 | E-GEOD-15297 | biostudies-arrayexpress
Project description:The diagnosis of Kawasaki disease (KD) is often difficult to distinguish from adenovirus (HAdV) and Group A streptococcal disease (GAS). We sought to: 1) to define the KD transcriptional signature that can aid in the diagnosis of complete and incomplete KD in children; 2) to identify specific biomarkers that objectively discriminate between KD and other mimicking conditions, including HAdV and 3) to test the prognostic utility of GEP to determine response to IVIG therapy and development of coronary artery lesions (CAL). Methods: Blood RNA samples were analyzed from 76 pediatric patients with complete KD, 13 with incomplete KD, 19 patients with HAdV, 17 patients with GAS disease, and age- and sex-matched healthy controls (HC). We used class comparisons (MW p< 0.01, Benjamini-Hochberg, and 1.25 fold change filter), class prediction, modular analysis and MDTH analyses to define the specificity of the KD profiles and identify markers of severity. Results: Statistical group comparisons identified 7,899 genes differentially expressed in 39 complete KD patients versus HC (KD biosignature). This signature was validated in another 37 patients with complete KD and in 13 patients with incomplete KD. Modular analysis in children with complete KD demonstrated overexpression of inflammation, neutrophils, myeloid cell, coagulation cascade, and cell cycle genes. The KNN class prediction algorithm identified 25-classifier genes that differentiated children with KD vs HAdV infection in two independent cohorts of patients with 96% (95% CI [80%-99%]) sensitivity and 95% [74%-99%] specificity. MDTH scores in KD patients significantly correlated with the baseline c-reactive protein (R=0.29, p=0.008) and was four fold higher than in children with HAdV (p<0.01). In addition, KD patients that remained febrile 36 hours after treatment with IVIG (non-responders) demonstrated higher baseline, pre-treatment MDTH values compared with responders [12,290 vs. 5,572 respectively; p=0.009]. Conclusion: Transcriptional signatures can be used as a tool to discriminate between KD and HAdV infection, and may also provide prognostic information.
2016-04-14 | GSE68004 | GEO