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Interleukin-9 release from human kidney grafts and its potential protective role in renal ischemia/reperfusion injury

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Abstract

Objective and design

The pathophysiology of ischemia/reperfusion (I/R) injury is dominated by an inflammatory response. In the identification of new therapeutic agents, the role of individual cytokines may be essential. Interleukin (IL)-9 is a pleiotropic cytokine recently identified to be involved in various immune responses. In this study, the role of IL-9 in renal I/R injury was assessed.

Methods

We performed repeated direct measurements of arteriovenous IL-9 concentration differences over the reperfused graft in human kidney transplantation.

Results

Substantial renal IL-9 release was observed from deceased donor kidneys (P = 0.006). In contrast, living donor kidneys, which have a more favourable clinical outcome, did not release IL-9 during early reperfusion (P = 0.78). Tissue expression of IL-9 did not change upon reperfusion in both living and deceased human donor kidneys. To assess the role of IL-9 in I/R injury, an experimental study comprising IL-9 inhibition in mice undergoing renal I/R was performed. Although there was no difference in kidney function, structural damage was significantly aggravated in anti-IL-9 treated mice.

Conclusions

Deceased donor grafts show a substantial IL-9 release upon reperfusion in clinical kidney transplantation. However, inhibition of IL-9 aggravated kidney damage, suggesting a regulating or minor role of IL-9 in clinical I/R injury.

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Acknowledgments

This work was financially supported by The Netherlands Organization for Health Research and Development (Project 92003525 to D.V.).

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Correspondence to Dorottya K. de Vries.

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Responsible Editor: Artur Bauhofer.

K. A. Kortekaas and D. K. de Vries contributed equally to this article.

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Kortekaas, K.A., de Vries, D.K., Reinders, M.E.J. et al. Interleukin-9 release from human kidney grafts and its potential protective role in renal ischemia/reperfusion injury. Inflamm. Res. 62, 53–59 (2013). https://doi.org/10.1007/s00011-012-0550-7

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  • DOI: https://doi.org/10.1007/s00011-012-0550-7

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