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Letter
Primed circulating monocytes are a source of IL-1β in patients with cirrhosis and ascites
  1. Sven Stengel1,
  2. Arndt Steube1,
  3. Nilay Köse-Vogel1,
  4. Tatiana Kirchberger-Tolstik1,
  5. Sachin Deshmukh2,
  6. Tony Bruns3
  1. 1Department of Internal Medicine IV, Jena University Hospital, Jena, Germany
  2. 2Center for Sepsis Control and Care, Jena University Hospital, Jena, Germany
  3. 3Department of Medicine III, University Hospital Aachen, Aachen, Germany
  1. Correspondence to Dr Tony Bruns, Department of Medicine III, University Hospital Aachen, Aachen 52074, Germany; tbruns{at}ukaachen.de

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We read with great interest the study of Monteiro and colleagues1 reporting the diagnostic significance and the prognostic relevance of elevated serum concentrations of interleukin (IL)-1α in compensated cirrhosis and IL-1β in recompensated cirrhosis. While we do agree that systemic inflammation is a major driver for the progression of liver disease and acute-on-chronic liver failure, caution is advised when interpreting serum IL-1β concentrations as evidence for underlying inflammasome activation causing complications of cirrhosis. Studies1–4 have been inconsistent about stage-dependent concentrations of circulating IL-1β in cirrhosis and acute-on-chronic liver failure (ACLF). Although some of these discrepancies can be attributed to differences in patients, cohort sizes, causes and severity of liver damage, the short serum half-life of cleaved IL-1β, and the sensitivity and specificity of the assays used, one major factor presumably affecting serum concentration is the cellular source of IL-1β and its mode of release.

The release of bioactive IL-1β from murine macrophages has first been described as a two-step activation dogma. While a first (priming) signal would be provided by pathogen-associated molecular patterns (PAMPs) or inflammatory cytokines in order to upregulate the inflammasome components, a second signal would …

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Footnotes

  • Twitter @tony_bruns

  • Contributors SS, AS, NK-V and TK-T performed the experiments and analyses. SS and TB wrote the manuscript. SD assisted with the experimental design and the writing of the manuscript. TB conceived of and supervised the study, obtained funding, provided guidance with experimental design and writing of the manuscript. All authors critically revised the manuscript for important intellectual content.

  • Funding This study was funded by German Research Foundation (DFG BR4182/3-1). German Federal Ministry of Education and Research (BMBF 01 E0 1502).

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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