ReviewEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology1994
Kinetics of tumour necrosis factor-alpha, soluble tumour necrosis factor receptors, interleukin 1-beta and its receptor antagonist during serious infections.
Review in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 39 citations in OpenAlex.
- A novel approach for emerging and antibiotic resistant infections: Innate defense regulators as an agnostic therapy.Journal of biotechnology · 2016Trial
- Nicotinamide does not influence cytokines or exhaled NO in human experimental endotoxaemia.Clinical and experimental immunology · 2004Trial
- Longitudinal measurements of inflammatory mediators in patients at risk of sepsis in the Emergency Department.Annals of intensive care · 2026Article
- Leptin's potential mechanisms in ICU-acquired weakness.Lipids in health and disease · 2025Review
- Involvement of Inflammasome Components in Kidney Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Transcriptomic changes in the large organs in lethal meningococcal shock are reflected in a porcine shock model.Frontiers in cellular and infection microbiology · 2022Article
- Out of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during Inflammation.Biomolecules · 2021Review
- Sepsis-Induced Immunosuppression in Neonates.Frontiers in pediatrics · 2018Review
- Deletion of Nlrp3 protects from inflammation-induced skeletal muscle atrophy.Intensive care medicine experimental · 2017Article
- Increased plasma levels of endozepines, endogenous ligands of benzodiazepine receptors, during systemic inflammation: a prospective observational study.Critical care (London, England) · 2014Observational
- Article
- Profile of blood cells and inflammatory mediators in periodic fever, aphthous stomatitis, pharyngitis and adenitis (PFAPA) syndrome.BMC pediatrics · 2010Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumour necrosis factor-alpha (TNF) and interleukin-1 beta (IL-1 beta) are the central mediators in the genesis of sepsis. The proinflammatory effects of these cytokines are counteracted in vivo by natural inhibitors. Soluble TNF receptors (sTNFR) are shed upon inflammatory stimuli such as IL-1 beta and TNF itself. Circulating TNF can be complexed by these receptors, thus preventing TNF from binding to effector cells. The binding of IL-1 beta to its receptor can be blocked by high concentrations of interleukin-1 receptor antagonist (IL-1Ra), which is produced and released upon nearly the same stimuli as IL-1 beta. This review presents some aspects of the kinetic behaviour of native sTNFR and of the production of native IL-1Ra during severe infections. It appears that in fulminant septicaemia, the plasma concentration of TNF is increased only transiently, during the very early stage of the infection. The concentration of sTNFR, in contrast, remains elevated much longer, probably due to a slower clearance. During the acute stage of severe infectious diseases, peripheral blood cells cannot be stimulated to produce IL-1 beta. The production of IL-1 Ra, in contrast, is not affected. Thus, the kinetic behaviour and regulation of TNF and IL-1 beta, is different from that of their antiinflammatory counterparts.
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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.