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Inhibition of Caspase-1 with Tetracycline Ameliorates Acute Lung Injury

  1. Author:
    Peukert, Konrad
    Fox, Mario
    Schulz, Susanne
    Feuerborn, Caroline
    Frede, Stilla
    Putensen, Christian
    Wrigge, Hermann
    Kummerer, Beate Mareike
    David, Sascha
    Seeliger, Benjamin
    Welte, Tobias
    Latz, Eicke
    Klinman,Dennis
    Wilhelm, Christoph
    Steinhagen, Folkert
    Bode, Christian

  2. Author Address

    Univ Hosp Bonn, Dept Anesthesiol & Intens Care Med, Venusberg Campus 1, D-53127 Bonn, Germany.Univ Hosp Bonn, Inst Virol, Bonn, Germany.Univ Hosp Bonn, Inst Innate Immun, Bonn, Germany.Univ Hosp Bonn, Inst Clin Chem & Clin Pharmacol, Bonn, Germany.Bergmannstrost Hosp Halle, Dept Anesthesiol Intens Care & Emergency Med, Pain Therapy, Halle, Germany.Hannover Med Sch, Dept Nephrol & Hypertens, Hannover, Germany.Hannover Med Sch, Dept Resp Med, Hannover, Germany.Hannover Med Sch, German Ctr Lung Res DZL, Hannover, Germany.Univ Hosp Zurich, Inst Intens Care Med, Zurich, Switzerland.NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
    1. Year: 2021
    2. Date: Jul 1
    3. Epub Date: 2021 Mar 22
  2. Journal: American Journal of Respiratory and Critical Care Medicine
  3. AMER THORACIC SOC,
    1. 204
    2. 1
    3. Pages: 53-63
  5. Type of Article: Article
  6. ISSN: 1073-449X
  1. Abstract:

    Rationale: Acute respiratory distress syndrome (ARDS) is a heterogeneous syndrome with a mortality of up to 40%. Precision medicine approaches targeting patients on the basis of their molecular phenotypes of ARDS might help to identify effective pharmacotherapies. The inflammasome-caspase-1 pathway contributes to the development of ARDS via IL-1 beta and IL-18 production. Recent studies indicate that tetracycline can be used to treat inflammatory diseases mediated by IL-1 beta and IL-18, although the molecular mechanism by which tetracycline inhibits inflammasome-caspase-1 signaling remains unknown.

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External Sources

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  2. DOI: 10.1164/rccm.202005-1916OC
  3. PMID: 33760701
  4. View record in Web of Science®
  5. WOS: 000674175600013

Library Notes

  1. Fiscal Year: FY2020-2021
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