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Putative function of goblet cells as epithelial sealing in ischaemia/reperfusion-induced intestinal barrier dysfunction
  1. Yuk Lung Wong1,
  2. Lars Hummitzsch1,
  3. Ingmar Lautenschläger1,
  4. Karina Zitta1,
  5. Thilo Wedel2,
  6. François Cossais2,
  7. Clemens Schafmayer3,
  8. Thomas Becker3,
  9. Rouven Berndt4,
  10. Matthias Gruenewald1,
  11. Norbert Weiler1,
  12. Markus Steinfath1,
  13. Martin Albrecht1
  1. 1 Department of Anesthesiology and Intensive Care Medicine, Universtiy Hospital Schleswig-Holstein, Kiel, Germany
  2. 2 Institute of Anatomy, University of Kiel, Kiel, Germany
  3. 3 Department of General and Thoracic Surgery, Universtiy Hospital Schleswig-Holstein, Kiel, Germany
  4. 4 Department of Cardiovascular Surgery, University Hospital Schleswig-Holstein, Kiel, Germany
  1. Correspondence to Professor Martin Albrecht, Department of Anesthesiology and Intensive Care Medicine, University Hospital Schleswig-Holstein, 24105 Kiel, Germany; martin.albrecht{at}uksh.de

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We read with great interest the article by Michael Camilleri who described in detail the important functions of goblet cells and the mucus component for intestinal barrier function.1 Apart from diseases resulting in intestinal inflammation and damage, intestinal ischaemia/reperfusion (I/R) injury also leads to epithelial cell damage, release of epithelial cells into the luminal space and as a consequence reduced barrier function.2–4 The latter enables bacterial translocation and in its severest form results in systemic inflammation and organ dysfunction.5 The fundamental importance of goblet cell secretory products in restricting bacterial translocation has also been reported previously in Gut by Grootjans et al who showed that colonic ischaemia leads to disruption of the mucus layer facilitating bacterial penetration into the underlying tissue and that this process is counteracted by increased secretory activity of goblet cells.6

We are currently performing a clinical trial in which the effects of remote ischaemic preconditioning …

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Footnotes

  • Contributors Study concept and design: YLW, LH, IL and MA. Practical implementation of experiments: TW, FC, CS, TB, KZ, LH and YLW. Data analyses and statistical analyses: KZ, YLW and MA. Writing of the manuscript: MA and YLW. Critical revision of the manuscript: RB, MS, TW and NW. All authors approved the final version for publication.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

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

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