ArticleAlcohol (Fayetteville, N.Y.)2019
Ethanol activates immune response in lymphoblastoid cells.
Article in Alcohol (Fayetteville, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Integrated single-cell multiomic profiling of caudate nucleus suggests key mechanisms in alcohol use disorder.Nature communications · 2025Article
- Next-generation biomarkers for alcohol consumption and alcohol use disorder diagnosis, prognosis, and treatment: A critical review.Alcohol, clinical & experimental research · 2025Review
- DNA-PK and ATM drive phosphorylation signatures that antagonistically regulate cytokine responses to herpesvirus infection or DNA damage.Cell systems · 2024Article
- 5. Collaborative Study on the Genetics of Alcoholism: Functional genomics.Genes, brain, and behavior · 2023Review
- RNA alternative splicing impacts the risk for alcohol use disorder.Molecular psychiatry · 2023Article
- Transcriptome-wide gene-gene interaction associations elucidate pathways and functional enrichment of complex traits.PLoS genetics · 2023Article
- Multi-omics signatures of alcohol use disorder in the dorsal and ventral striatum.Translational psychiatry · 2022Article
- RNA biomarkers for alcohol use disorder.Frontiers in molecular neuroscience · 2022Review
- A pan-cancer analysis revealed the role of the SLC16 family in cancer.Channels (Austin, Tex.) · 2021Article
- Effects of chronic intermittent ethanol exposure and withdrawal on neuroblastoma cell transcriptome.Alcohol (Fayetteville, N.Y.) · 2020Article
- Monocarboxylate Transporters (SLC16): Function, Regulation, and Role in Health and Disease.Pharmacological reviews · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.