ArticleMediators of inflammation2020
Sustained Immunoparalysis in Endotoxin-Tolerized Monocytic Cells.
Article in Mediators of inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Post-Transplant Sepsis After Liver Transplantation: Clinical Characteristics and Therapeutic Challenges.Journal of clinical medicine · 2026Review
- Akkermansia muciniphila attenuates sepsis-induced immunosuppression by shaping endotoxin-tolerant macrophage phenotypes.Pathogens and disease · 2025Article
- USP3 plays a critical role in the induction of innate immune tolerance.EMBO reports · 2023Article
- Whey protein hydrolysate mitigates both inflammation and endotoxin tolerance in THP-1 human monocytic leukemia cells.Immunity, inflammation and disease · 2022Article
- Review
- PARP Traps Rescue the Pro-Inflammatory Response of Human Macrophages in the In Vitro Model of LPS-Induced Tolerance.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Role of IL-37- and IL-37-Treated Dendritic Cells in Acute Coronary Syndrome.Oxidative medicine and cellular longevity · 2021Review
- Mammary leukocytes function of endotoxin tolerant goat induced by intrauterine infusion of lipopolysaccharide.Innate immunityArticle
- Vancomycin and daptomycin modulate the innate immune response in a murine model of LPS-induced sepsis.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is associated with a strong inflammatory reaction triggering a complex and prolonged immune response. Septic patients have been shown to develop sustained immunosuppression due to a reduced responsiveness of leukocytes to pathogens. Changes in cellular metabolism of leukocytes have been linked to this phenomenon and contribute to the ongoing immunological derangement. However, the underlying mechanisms of these phenomena are incompletely understood. In cell culture models, we mimicked LPS tolerance conditions to provide evidence that epigenetic modifications account for monocyte metabolic changes which cause immune paralysis in restimulated septic monocytes. In detail, we observed differential methylation of CpG sites related to metabolic activity in human PBMCs 18 h after septic challenge. The examination of changes in immune function and metabolic pathways was performed in LPS-tolerized monocytic THP-1 cells. Passaged THP-1 cells, inheriting initial LPS challenge, presented with dysregulation of cytokine expression and oxygen consumption for up to 7 days after the initial LPS treatment. Proinflammatory cytokine concentrations of TNF
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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.