ETHANOL ACTIVATES IMMUNE RESPONSE IN LYMPHOBLASTOID CELLS
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA521555 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8552380.fastq.gz | Fastqsanger.gz | |||
| SRR8552390.fastq.gz | Fastqsanger.gz | |||
| SRR8552400.fastq.gz | Fastqsanger.gz | |||
| SRR8552410.fastq.gz | Fastqsanger.gz | |||
| SRR8552420.fastq.gz | Fastqsanger.gz |
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Project description:The short term effects of alcohol on gene expression in brain tissue cannot directly be studied in humans. Because neuroimmune signaling is altered by alcohol, immune cells are a logical, accessible choice to study and might provide biomarkers. RNAseq was used to study the effects of 48 h exposure to ethanol on lymphoblastoid cell lines (LCLs) from 20 alcoholics and 20 controls. Ethanol exposure resulted in differential expression of 4,577 of the 12,526 genes detectably expressed in the LCLs (FDR ≤ 0.05); 55% of these showed increased expression. Cells from alcoholics and controls responded similarly. Ingenuity pathway analysis identified several pathways in which expression was altered: NFkB, neuroinflammation, IL8, and dendritic cell maturation pathways were activated, consistent with increased signaling by NFkB, TNF, IL1, IL4, IL18, TLR4, and LPS. Signaling by Interferons A and B decreased, as did EIF2 signaling, phospholipase C signaling and Glycolysis. Baseline gene expression patterns were similar in LCLs from alcoholics and controls. At relaxed stringency (p<0.05), 438 genes differed, 223 of which were also affected by ethanol. There was a suggestion of compensation because baseline differences (no ethanol) were in the opposite direction of differences due to ethanol exposure in 75% of these genes. Ingenuity Pathway analysis Identified pathways wAldosterone, phospholipase C, and opioid signaling as significant. The pattern of expression was consistent with increased signaling by several cytokines including interferons, and TLR2 and 3 in alcoholics. Expression of genes in the cholesterol biosynthesis pathway including the rate-limiting enzyme HMGCR was lower in alcoholics.
2019-03-25 | GSE126329 | GEO
Project description:The short-term effects of alcohol on gene expression in brain tissue cannot directly be studied in humans. Because neuroimmune signaling is altered by alcohol, immune cells are a logical, accessible choice to study and may provide biomarkers. RNAseq was used to study the effects of 48-h exposure to ethanol on lymphoblastoid cell lines (LCLs) from 20 alcoholic subjects and 20 control subjects. Ethanol exposure resulted in differential expression of 4456 of the 12,503 genes detectably expressed in the LCLs (FDR [false discovery rate] ≤ 0.05); 52% of these showed increased expression. Cells from alcoholic subjects and control subjects responded similarly. The genes whose expression changed fell into many pathways: NFκB, neuroinflammation, IL6, IL2, IL8, and dendritic cell maturation pathways were activated, consistent with increased signaling by NFκB, TNF, IL1, IL4, IL18, TLR4, and LPS. Signaling by Interferons A and B decreased, as did EIF2 signaling, phospholipase C signaling, and glycolysis. Baseline gene expression patterns were similar in LCLs from alcoholic subjects and control subjects. At relaxed stringency (p < 0.05), 465 genes differed, 230 of which were also affected by ethanol. There was a suggestion of compensation because baseline differences (no ethanol) were in the opposite direction of differences due to ethanol exposure in 78% of these genes. Pathways with IL8, phospholipase C, and α-adrenergic signaling were significant. The pattern of expression was consistent with increased signaling by several cytokines, including interferons, TLR2, and TLR3 in alcoholics. Expression of genes in the cholesterol biosynthesis pathway, including the rate-limiting enzyme HMGCR, was lower in alcoholic subjects. LCLs show many effects of ethanol exposure, some of which might provide biomarkers for alcohol use disorders. Identifying genes and pathways altered by ethanol can aid in interpreting which genes within loci identified by GWAS might play functional roles.
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Project description:Compared gene expression in lymphoblasoid cell lines from alcholics and controls and 24 hr treatment with ethanol. To elucidate the effects of a controlled exposure to ethanol on gene expression, we studied lymphoblastoid cell lines (LCLs) from 21 alcoholics and 21 controls. We cultured each cell line for 24 h with and without 75 mM ethanol and measured gene expression using microarrays. Differences in expression between LCL from alcoholics and controls were modest, but included 13 genes previously identified as associated with alcoholism or related traits in one or more GWAS, including KCNA3, DICER1, ZNF415, Catalase and PPARGC1B. The paired design allowed us to detect very small changes due to ethanol treatment: ethanol altered the expression of 37% of the probe sets (51% of the unique named genes) detectably expressed in these LCLs, but most by very modest amounts. 99% of the named genes expressed in the LCLs were also expressed in at least 1 of 9 brain regions tested, suggesting that LCLs are a reasonable and accessible proxy for brain tissues. Key pathways affected by ethanol include cytokine, TNF and NF-kB signaling. Among the genes affected by ethanol were ANK3, EPHB1, SLC1A1, SLC9A9, NRD1, and SH3BP5, which were reported to be associated with alcoholism or related phenotypes in 2 genome wide association studies. Genes that either differed in expression between alcoholics and controls or were affected by ethanol exposure are candidates for further study.
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2005-12-03 | GSE3727 | GEO
Project description:Compared gene expression in lymphoblasoid cell lines from alcholics and controls and 24 hr treatment with ethanol. To elucidate the effects of a controlled exposure to ethanol on gene expression, we studied lymphoblastoid cell lines (LCLs) from 21 alcoholics and 21 controls. We cultured each cell line for 24 h with and without 75 mM ethanol and measured gene expression using microarrays. Differences in expression between LCL from alcoholics and controls were modest, but included 13 genes previously identified as associated with alcoholism or related traits in one or more GWAS, including KCNA3, DICER1, ZNF415, Catalase and PPARGC1B. The paired design allowed us to detect very small changes due to ethanol treatment: ethanol altered the expression of 37% of the probe sets (51% of the unique named genes) detectably expressed in these LCLs, but most by very modest amounts. 99% of the named genes expressed in the LCLs were also expressed in at least 1 of 9 brain regions tested, suggesting that LCLs are a reasonable and accessible proxy for brain tissues. Key pathways affected by ethanol include cytokine, TNF and NF-kB signaling. Among the genes affected by ethanol were ANK3, EPHB1, SLC1A1, SLC9A9, NRD1, and SH3BP5, which were reported to be associated with alcoholism or related phenotypes in 2 genome wide association studies. Genes that either differed in expression between alcoholics and controls or were affected by ethanol exposure are candidates for further study. Lymphoblastoid cells from 21 alcoholics and 21 controls were treated with 75mM ethanol for 24 hours.
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Project description:The nematode shows responses to acute ethanol exposure that are similar to those observed in humans, mice, and Drosophila, namely hyperactivity followed by uncoordination and sedation. We used in this report the nematode Caenorhabditis elegans as a model system to identify and characterize the genes that are affected by ethanol exposure and to link those genes functionally into an ethanol-induced gene network. By analyzing the expression profiles of all C. elegans ORFs using microarrays, we identified 230 genes affected by ethanol. While the ethanol response of some of the identified genes was significant at early time points, that of the majority was at late time points, indicating that the genes in the latter case might represent the physiological consequence of the ethanol exposure. We further characterized the early response genes that may represent those involved directly in the ethanol response. These genes included many heat shock protein genes, indicating that high concentration of ethanol acts as a strong stress to the animal. Interestingly, we identified two non-heat-shock protein genes that were specifically responsive to ethanol. glr-2 was the only glutamate receptor gene to be induced by ethanol. T28C12.4, which encodes a protein with limited homology to human neuroligin, was also specific to ethanol stress. Finally, by analyzing the promoter regions of the early response genes, we identified a regulatory element, TCTGCGTCTCT, that was necessary for the expression of subsets of ethanol response genes. Groups of assays that are related as part of a time series. Computed
2005-12-02 | E-GEOD-3727 | biostudies-arrayexpress