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Novel in vitro model for studying ureteric stent-induced cell injury

  1. Chelsea N. Elwood1,4,
  2. Dirk Lange4,
  3. Richard Nadeau1,
  4. Shannon Seney1,
  5. Kelly Summers1,3,
  6. Ben H. Chew4,
  7. John D. Denstedt1,2,
  8. Peter A. Cadieux1,2,3,*

Article first published online: 3 NOV 2009

DOI: 10.1111/j.1464-410X.2009.09001.x

Issue

BJU International

BJU International

Volume 105, Issue 9, pages 1318–1323, May 2010

Additional Information

How to Cite

Elwood, C. N., Lange, D., Nadeau, R., Seney, S., Summers, K., Chew, B. H., Denstedt, J. D. and Cadieux, P. A. (2010), Novel in vitro model for studying ureteric stent-induced cell injury. BJU International, 105: 1318–1323. doi: 10.1111/j.1464-410X.2009.09001.x

Author Information

  1. 1

    Lawson Health Research Institute, Departments of

  2. 2

    Surgery and

  3. 3

    Microbiology and Immunology, University of Western Ontario, London, Ontario and

  4. 4

    The Stone Centre at Vancouver General Hospital, University of British Columbia, Vancouver, British Columbia, Canada

*Peter A. Cadieux, F0-102a Lawson Health Research Institute, 268 Grosvenor St. London, Ontario, Canada N6A 4V2. e-mail: pcadieux@uwo.ca

Publication History

  1. Issue published online: 9 APR 2010
  2. Article first published online: 3 NOV 2009
  3. Accepted for publication 14 July 2009

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Keywords:

  • stent;
  • cytokines;
  • inflammation;
  • triclosan;
  • cell line

OBJECTIVE

To develop a novel in vitro model for the study of bladder and kidney epithelial cell injury akin to stent movement, as ureteric stents are associated with urinary tract complications that can significantly add to patient morbidity. These sequelae may be linked to inflammation triggered by stent-mediated mechanical injury to the urinary tract.

MATERIALS AND METHODS

T24 bladder and A498 kidney cell line monolayers were damaged mechanically by segments of either Percuflex Plus® (PP) or Triumph® (triclosan-eluting) stents (both from Boston Scientific Corporation Inc. Natick, MA, USA) and the resulting expression profiles of several pro-inflammatory cytokines and growth factors were analysed.

RESULTS

After control injury using the PP stent, supernatants of both cell lines had significantly increased levels of interleukin (IL)-6, IL-8, basic fibroblast growth factor and platelet-derived growth factor BB, and A498 cells also had increased tumour necrosis factor α. In almost all cases, the presence of triclosan within the media abrogated the pro-inflammatory cytokine increases, while its effects on growth factors varied.

CONCLUSION

This study suggests that stent-related symptoms in the bladder and kidney may be partially due to a local inflammatory response to epithelial damage caused by the presence and movement of the stent. Future stent design should take these inflammatory responses, with respect to physical injury, into consideration, using either more biocompatible materials or anti-inflammatory compounds such as triclosan.

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