ArticleThe Journal of experimental medicine1994
A labile transcriptional repressor modulates endotoxin tolerance.
Article in The Journal of experimental medicine, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 113 citations in OpenAlex.
- Modulation of TNF-α mRNA stability by human antigen R and miR181s in sepsis-induced immunoparalysis.EMBO molecular medicine · 2015Trial
- Effects of a fish oil containing lipid emulsion on plasma phospholipid fatty acids, inflammatory markers, and clinical outcomes in septic patients: a randomized, controlled clinical trial.Critical care (London, England) · 2010Trial
- HDAC3 Mediates the Inflammatory Response and LPS Tolerance in Human Monocytes and Macrophages.Frontiers in immunology · 2020Article
- Responses of perivascular macrophages to circulating lipopolysaccharides in the subfornical organ with special reference to endotoxin tolerance.Journal of neuroinflammation · 2019Article
- Pyruvate dehydrogenase complex stimulation promotes immunometabolic homeostasis and sepsis survival.JCI insight · 2018Article
- AMP-Activated Protein Kinase and Glycogen Synthase Kinase 3β Modulate the Severity of Sepsis-Induced Lung Injury.Molecular medicine (Cambridge, Mass.) · 2016Article
- GAPDH Binding to TNF-α mRNA Contributes to Posttranscriptional Repression in Monocytes: A Novel Mechanism of Communication between Inflammation and Metabolism.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Processing Body Formation Limits Proinflammatory Cytokine Synthesis in Endotoxin-Tolerant Monocytes and Murine Septic Macrophages.Journal of innate immunity · 2015Article
- Notch Signaling Pathway Was Involved in Regulating Programmed Cell Death 1 Expression during Sepsis-Induced Immunosuppression.Mediators of inflammation · 2015Article
- Upregulating nonneuronal cholinergic activity decreases TNF release from lipopolysaccharide-stimulated RAW264.7 cells.Mediators of inflammation · 2014Article
- RelB: an outlier in leukocyte biology.Journal of leukocyte biology · 2013Review
- Mitogen-activated protein kinase phosphatase 1 disrupts proinflammatory protein synthesis in endotoxin-adapted monocytes.Clinical and vaccine immunology : CVI · 2013Article
- MicroRNA-146a and RBM4 form a negative feed-forward loop that disrupts cytokine mRNA translation following TLR4 responses in human THP-1 monocytes.Immunology and cell biology · 2013Article
- NAD+-dependent sirtuin 1 and 6 proteins coordinate a switch from glucose to fatty acid oxidation during the acute inflammatory response.The Journal of biological chemistry · 2012Article
- MicroRNA-146a regulates both transcription silencing and translation disruption of TNF-α during TLR4-induced gene reprogramming.Journal of leukocyte biology · 2011Article
- Epigenetics, bioenergetics, and microRNA coordinate gene-specific reprogramming during acute systemic inflammation.Journal of leukocyte biology · 2011Review
- MicroRNA in TLR signaling and endotoxin tolerance.Cellular & molecular immunology · 2011Review
- Mechanistic role of microRNA-146a in endotoxin-induced differential cross-regulation of TLR signaling.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Facultative heterochromatin formation at the IL-1 beta promoter in LPS tolerance and sepsis.Cytokine · 2011Article
- MicroRNAs distinguish translational from transcriptional silencing during endotoxin tolerance.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tolerance to bacterial lipopolysaccharide (LPS, endotoxin) is an adaptive cellular process whereby exposure to endotoxin induces a subsequent hyporesponsive state characterized by decreased levels of LPS-induced cytokine mRNA and protein. We demonstrate, in a human promonocytic cell line, THP-1, that endotoxin tolerance is manifested by decreased LPS-induced interleukin 1 beta (IL-1 beta) transcription. Inhibition of protein synthesis reverses the tolerant phenotype by inducing transcription of IL-1 beta in the absence of a second stimulus. These results indicate that a labile protein contributes to the endotoxin-tolerant phenotype, and that this factor acts in a dominant repressive manner to inhibit the activity of existing transcription factors. We provide further data that cellular expression of I kappa B-alpha correlates with downregulated IL-1 beta gene expression during endotoxin tolerance, implicating I kappa B-alpha as a potential candidate for the labile repressor identified herein.
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.