Elevated Levels of Circulating Transforming Growth Factor-β 1 in Patients with the Sepsis Syndrome
Authors: Christelle Marie
Journal: Annals of Internal Medicine (1996)

Letters15 September 1996Elevated Levels of Circulating Transforming Growth Factor-β 1 in Patients with the Sepsis SyndromeChristelle Marie, MSc, Jean-Marc Cavaillon, PhD, and Marie-Reine Losser, MDChristelle Marie, MScInstitut Pasteur, Paris, FranceHopital Lariboisiere, Paris, France, Jean-Marc Cavaillon, PhDInstitut Pasteur, Paris, FranceHopital Lariboisiere, Paris, France, and Marie-Reine Losser, MDInstitut Pasteur, Paris, FranceHopital Lariboisiere, Paris, FranceAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-125-6-199609150-00034 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:The sepsis syndrome is associated with the presence of circulating proinflammatory cytokines. Recent investigations have indicated the presence of naturally occurring antiinflammatory mediators (such as interleukin-1ra, soluble tumor necrosis factor receptor [sTNF R], and interleukin-10). Among the anti-inflammatory cytokines, transforming growth factor-β 1 (TGF-β 1) has been shown to repress the production of inflammatory cytokines by activated macrophages [1] and to induce the release of sTNF R and interleukin-1ra [2]. Circulating TGF-β 1 levels are present in healthy persons, and the role of TGF-β 1 in homeostasis has been clearly established in knock-out mice, which die within ...References1. Bogdan C, Nathan C. Modulations of macrophage function by transforming growth factor-β, interleukin-4 and interleukin-10. Ann N Y Acad Sci. 1993; 685:713-39. Google Scholar2. Turner M, Chantry D, Katsikiq P, Berger A, Brennan FM, Feldman M. Induction of the interleukin-1 receptor antagonist protein by transforming growth factor-β. Eur J Immunol. 1991; 21:1635-9. Google Scholar3. Shull MM, Ormsby I, Kier AB, Pawlowski S, Diebold RJ, Yin M, et al. Targeted disruption of the mouse transforming growth factor-β 1 gene results in multifocal inflammatory disease. Nature. 1992; 359:693-9. Google Scholar4. Miller-Graziano CL, Szabo G, Griffey K, Mehta B, Kodys K, Catalano D. Role of elevated monocyte transforming growth factor-β production in post-trauma immunosuppression. J Clin Immunol. 1991; 11:95-102. Google Scholar5. Pasteur L. Compte Rendu de la Seance l'Academie des Sciences. 3 May 1880. Google Scholar Author, Article, and Disclosure InformationAuthors: Christelle Marie, MSc; Jean-Marc Cavaillon, PhD; Marie-Reine Losser, MDAffiliations: Institut Pasteur, Paris, FranceHopital Lariboisiere, Paris, France PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byOut of Control: The Role of the Ubiquitin Proteasome System in Skeletal Muscle during InflammationPotential Targets to Mitigate Trauma- or Sepsis-Induced Immune SuppressionCorrection of immunosuppression in aged septic rats by human ghrelin and growth hormone through the vagus nerve-dependent inhibition of TGF-β productionTGF-β Pathway Inhibition Protects the Diaphragm From Sepsis-Induced Wasting and Weakness in RatImmunotherapy in sepsis - brake or accelerate?Immunosuppression is Inappropriately Qualifying the Immune Status of Septic and SIRS PatientsSecreted Frizzled-Related Protein 2 and Inflammation-Induced Skeletal Muscle AtrophyImmunotherapy: A promising approach to reverse sepsis-induced immunosuppressionTargeting cytokines as a treatment for patients with sepsis: A lost cause or a strategy still worthy of pursuit?Effect of BML-111 on the intestinal mucosal barrier in sepsis and its mechanism of actionHost Response Biomarkers in the Diagnosis of Sepsis: A General OverviewDifferences Between Murine and Human SepsisRéponse inflammatoire et anti-inflammatoire de l'hôte au cours du sepsisExpression and Function of Transforming Growth Factor β in MelioidosisMédiateurs de l'inflammation au cours du sepsisSMAD4 Is Required for Development of Maximal Endotoxin ToleranceTransforming growth factor-β1 blocks in vitro cardiac myocyte depression induced by tumor necrosis factor-α, interleukin-1β, and human septic shock serumCytokines and Escherichia coli SepsisInvited review: Compartmentalization of the inflammatory response in sepsis and SIRSSophorolipids block lethal effects of septic shock in rats in a cecal ligation and puncture model of experimental sepsis*Hepatic over-expression of TGF-beta1 promotes LPS-induced inflammatory cytokine secretion by liver cells and endotoxemic shockThe bovine innate immune response during experimentally-induced Pseudomonas aeruginosa mastitisPatients with acute on chronic liver failure display 'sepsis-like' immune paralysisLongitudinal study of cytokine and immune transcription factor mRNA expression in septic shockTGF-β: the perpetrator of immune suppression by regulatory T cells and suicidal T cellsCytokine modulation in sepsis and septic shockInvolvement of Pro- and Anti-Inflammatory Cytokines in SepsisThe Pro-Inflammatory Cytokine CascadeInhibitory CytokinesMyocardial dysfunction in septic shock: Part II. 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