LPS inflammation model and thalidomide effect using PBMC cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE28708 | GEO | 2011/09/30
SECONDARY ACCESSION(S): PRJNA139003
REPOSITORIES: GEO
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Project description:In this research, we use DNA microarray analysis to clarify the gene expression responses from thalidomide in PBMC cells after lipopolysaccharide (LPS) treatment. Analysis used PBMC as control samples for comparison to the experimental samples: PBMC stimulated with LPS and PBMC stimulated with LPS treated with LPS. Indirect comparisons were made across multiple arrays with raw data pulled from different channels for data analysis and comparison to the control data.
2011-09-29 | E-GEOD-28708 | biostudies-arrayexpress
Project description:Thalidomide Exerts Distinct Molecular Antileukemic Effects and Combined Thalidomide/Fludarabine Therapy is Clinically Effective in High-Risk Chronic Lymphocytic Leukemia Background: Thalidomide represents a promising immunomodulatory drug that targets both leukemia cells and the tumor microenvironment. Methods: We treated chronic lymphocytic leukemia (CLL) patients with a combined thalidomide/fludarabine regimen and monitored cellular and molecular changes induced by thalidomide in-vivo prior to fludarabine treatment. Thalidomide was given daily (100mg p.o./day) and fludarabine was administered on days 7-11 (25 mg/m² i.v./day) within each 4-week cycle (maximum of 6 cycles). Twenty patients received thalidomide/fludarabine as first line therapy and 20 patients were previously treated. Unmutated IgVH mutation status was found in 36 cases and 13 had high-risk cytogenetic aberrations (deletion of 17p13 or 11q22-q23). Results: The overall response rate was 80% and 25% for untreated and previously treated patients, respectively. While thalidomide effectively reduced the number of CLL cells, the number of CD3 lymphocytes showed no significant change, but the number of CD4+CD25hiFOXP3+ T-regulatory cells was significantly decreased. Gene expression profiling revealed a thalidomide induced signature containing both targets known to play a role in immunomodulatory drug action as well as novel candidate genes. Conclusions: Combined thalidomide/fludarabine therapy demonstrated efficacy in high-risk CLL patients. Furthermore, our study provides novel biological insights into thalidomide effect, which might act by enhancing apoptosis of CLL cells and reducing Tregs, thereby enabling T-cell dependent anti-tumor effect.
2009-08-21 | GSE15913 | GEO
Project description:LPS inflammation model and thalidomide effect using PBMC cells
| PRJNA139003 | ENA
Project description:Genipin is a natural blue colorant in food industry. Inflammation is correlated with human disorders, and nuclear factor-κB (NF-κB) is the critical molecule involved in inflammation. In this study, the anti-inflammatory effect of genipin on the lipopolysaccharide (LPS)-induced acute systemic inflammation in mice was evaluated by NF-κB bioluminescence-guided transcriptomic analysis. Transgenic mice carrying the NF-κB-driven luciferase genes were administered intraperitoneally with LPS and various amounts of genipin. Bioluminescent imaging showed that genipin significantly suppressed LPS-induced NF-κB-dependent luminescence in vivo. The suppression of LPS-induced acute inflammation by genipin was further evidenced by the reductions of cytokine levels in sera and organs. Microarray analysis of these organs showed that the transcripts of 79 genes were differentially expressed in both LPS and LPS/genipin groups, and one third of these genes belonged to chemokine ligand, chemokine receptor, and interferon (IFN)-induced protein genes. Moreover, network analysis showed that NF-κB played a critical role in the regulation of genipin-affected gene expression. In conclusion, we newly identified that genipin exhibited anti-inflammatory effects in a model of LPSinduced acute systemic inflammation via downregulation of chemokine ligand, chemokine receptor, and IFN-induced protein productions. A total of 25 transgenic mice (female, 6 to 8 weeks old) were randomly divided into five groups of five mice: (1) mock, no treatment; (2) LPS (4 mg/kg), (3) LPS plus genipin (1 mg/kg), (4) LPS plus genipin (10 mg/kg), and (5) LPS plus genipin (100 mg/kg). Mice were challenged intraperitoneally with LPS and then with genipin 10 min later. Four hours later, mice were imaged for the luciferase activity, and subsequently sacrificed for ex vivo imaging, RNA extraction, and immunohistochemical staining.
2012-02-25 | E-GEOD-35934 | biostudies-arrayexpress
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2016-02-25 | E-GEOD-76561 | biostudies-arrayexpress
Project description:Wild-type bone marrow-derived macrophages (BMDMs) were treated with vehicle (0.1% EtOH/D-PBS), 6h 100 ng/ml lipopolysaccharide (LPS) or 16h 1uM dexamethasone (Dex) and 6h 100 ng/ml LPS (Dex+LPS) and mRNA expression analysed by RNA-Seq.
2020-12-31 | GSE137412 | GEO
Project description:Genipin is a natural blue colorant in food industry. Inflammation is correlated with human disorders, and nuclear factor-κB (NF-κB) is the critical molecule involved in inflammation. In this study, the anti-inflammatory effect of genipin on the lipopolysaccharide (LPS)-induced acute systemic inflammation in mice was evaluated by NF-κB bioluminescence-guided transcriptomic analysis. Transgenic mice carrying the NF-κB-driven luciferase genes were administered intraperitoneally with LPS and various amounts of genipin. Bioluminescent imaging showed that genipin significantly suppressed LPS-induced NF-κB-dependent luminescence in vivo. The suppression of LPS-induced acute inflammation by genipin was further evidenced by the reductions of cytokine levels in sera and organs. Microarray analysis of these organs showed that the transcripts of 79 genes were differentially expressed in both LPS and LPS/genipin groups, and one third of these genes belonged to chemokine ligand, chemokine receptor, and interferon (IFN)-induced protein genes. Moreover, network analysis showed that NF-κB played a critical role in the regulation of genipin-affected gene expression. In conclusion, we newly identified that genipin exhibited anti-inflammatory effects in a model of LPSinduced acute systemic inflammation via downregulation of chemokine ligand, chemokine receptor, and IFN-induced protein productions.
2012-02-25 | GSE35934 | GEO
Project description:PBMC were exposed to Cell Free Nucleic Acids (CFNA) extracted from blood products eligible for transfusion: Red Blood Cell units (RBC), Fresh Frozen Plasma units (FFP). PBMC alone exposed to the same extract from PBS were used as a control (PBMC+control). PBMC alone were also used as control. The used positive control was PBMC exposed to Lipopolysaccharide (LPS)
2017-09-22 | GSE104107 | GEO
Project description:All samples were gathered from mouse RAW 264.7 cells (macrophages). Control total RNA was extracted from untreated RAW 264.7 cells cultured for either 1, 2, 4, 8, 16 or 48 hours. Test total RNA was extracted from lipopolysaccharide (100ng/ml) and lipopolysaccharide-binding protein (100pM) treated RAW 264.4 cells cultured for either 1, 2, 4, 8, 16 or 48 hours. This SuperSeries is composed of the following subset Series: GSE1099: Effect of LPS and LPS-binding protein treatment for 1 hour on RAW 264.4 cells GSE1100: Effect of LPS and LPS-binding protein treatment for 2 hours on RAW 264.4 cells GSE1101: Effect of LPS and LPS-binding protein treatment for 4 hours on RAW 264.4 cells GSE1102: Effect of LPS and LPS-binding protein treatment for 8 hours on RAW 264.4 cells GSE1103: Effect of LPS and LPS-binding protein treatment for 16 hours on RAW 264.4 cells GSE1104: Effect of LPS and LPS-binding protein treatment for 48 hours on RAW 264.4 cells Refer to individual Series
2004-03-04 | E-GEOD-1098 | biostudies-arrayexpress
Project description:To unravel the mechanisms of thalidomide developmental toxicity, we used microarrays to study transcriptomic changes induced by thalidomide during mouse embryonic stem cell (mESC) differentiation. C57BL/6 mESCs were allowed to differentiate spontaneously and global gene expression changes were studied using microarrays at at different time points after exposure to 0.25 mM thalidomide (THD).
2015-05-31 | GSE61306 | GEO