ArticleJournal of immunology (Baltimore, Md. : 1950)2009
The opposite effects of acute and chronic alcohol on lipopolysaccharide-induced inflammation are linked to IRAK-M in human monocytes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 1 of them a synthesis that pooled it.
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
126 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.
- Pooled it
- Acute changes in immune biomarkers under low- and moderate-dose alcohol in light and heavy drinkers: A randomized, placebo-controlled trial.Alcohol, clinical & experimental research · 2025Trial
- Comorbidities and Inflammation: How Chronic Diseases Prime the Host Response in Sepsis.International journal of molecular sciences · 2026Review
- Ethanol exacerbates post-burn neuroinflammation and gut-brain barrier dysfunction which are associated with microbiome changes.Alcohol (Fayetteville, N.Y.) · 2026Review
- Strongyloides stercoralis infection alters liver enzyme levels in alcoholic patientsBiomedica : revista del Instituto Nacional de Salud · 2026Article
- Serum HMGB1 and Alcohol-Related Liver Disease.Journal of clinical medicine · 2026Article
- Alcohol-induced susceptibility to pulmonary bacterial infections: A narrative review.Alcohol, clinical & experimental research · 2025Review
- Alcohol consumption and immune cell profiles: Insights from the Framingham Heart Study.Alcohol, clinical & experimental research · 2025Article
- Review
- Short-term heavy drinking in a non-human primate model skews monocytes toward a hypo-inflammatory phenotype.Frontiers in immunology · 2025Article
- Role of Myeloid Cell-Specific Adenylyl Cyclase Type 7 in Lipopolysaccharide- and Alcohol-Induced Immune Responses.International journal of molecular sciences · 2024Article
- Linking alcohol use to Alzheimer's disease: Interactions with aging and APOE along immune pathways.Medical research archives · 2024Article
- The Role of Cytokines in the Pathogenesis and Treatment of Alcoholic Liver Disease.Diseases (Basel, Switzerland) · 2024Review
- Adolescent intermittent ethanol (AIE) produces lasting, sex-specific changes in rat body fat independent of changes in white blood cell composition.Frontiers in physiology · 2024Article
- Exacerbating effects of single-dose acute ethanol exposure on neuroinflammation and amelioration by GPR110 (ADGRF1) activation.Journal of neuroinflammation · 2023Article
- Direct and indirect effects of alcohol and its toxic metabolite acetaldehyde on human esophageal myofibroblasts and epithelial cells.Alcohol, clinical & experimental research · 2023Article
- Mitochondrial Dysfunction: At the Nexus between Alcohol-Associated Immunometabolic Dysregulation and Tissue Injury.International journal of molecular sciences · 2023Review
- Prenatal and adolescent alcohol exposure programs immunity across the lifespan: CNS-mediated regulation.Pharmacology, biochemistry, and behavior · 2022Review
- HCV and tumor-initiating stem-like cells.Frontiers in physiology · 2022Review
- An exploratory study of pro-inflammatory cytokines in individuals with alcohol use disorder: MCP-1 and IL-8 associated with alcohol consumption, sleep quality, anxiety, depression, and liver biomarkers.Frontiers in psychiatry · 2022Article
66 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Impaired host defense after alcohol use is linked to altered cytokine production, however, acute and chronic alcohol differently modulate monocyte/macrophage activation. We hypothesized that in human monocytes, acute alcohol induces hyporesponsiveness to LPS, resulting in decreased TNF-alpha, whereas chronic alcohol increases TNF-alpha by sensitization to LPS. We found that acute alcohol increased IL-1R-associated kinase-monocyte (IRAK-M), a negative regulator of IRAK-1, in human monocytes. This was associated with decreased IkappaB alpha kinase activity, NFkappaB DNA binding, and NFkappaB-driven reporter activity after LPS stimulation. In contrast, chronic alcohol decreased IRAK-M expression but increased IRAK-1 and IKK kinase activities, NFkappaB DNA binding, and NFkappaB-reporter activity. Inhibition of IRAK-M in acute alcohol-exposed monocytes using small interfering RNA restored the LPS-induced TNF-alpha production whereas over-expression of IRAK-M in chronic alcohol macrophages prevented the increase in TNF-alpha production. Addition of inhibitors of alcohol metabolism did not alter LPS signaling and TNF-alpha production during chronic alcohol exposure. IRAK-1 activation induces MAPKs that play an important role in TNF-alpha induction. We determined that acute alcohol decreased but chronic alcohol increased activation of ERK in monocytes and ERK inhibitor, PD98059, prevented the chronic alcohol-induced increase in TNF-alpha. In summary, inhibition of LPS-induced NFkappaB and ERK activation by acute alcohol leads to hyporesponsiveness of monocytes to LPS due to increased IRAK-M. In contrast, chronic alcohol sensitizes monocytes to LPS through decreased IRAK-M expression and activation of NFkappaB and ERK kinases. Our data indicate that IRAK-M is a central player in the opposite regulation of LPS signaling by different lengths of alcohol exposure in monocytes.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.