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EUROPEAN RESPIRATORY REVIEW, 2006;15: 168-169. doi:10.1183/09059180.00010108
© 2006 the European Respiratory Society
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The molecular controls of resolution of inflammation: what can we learn from zebrafish?

StephenA. Renshaw, MA, MRCP, PhD*, CatherineA. Loynes, BSc*, DanielM. Trushell*, PhilipW. Ingham, FRS# and MoiraK. B. Whyte, FRCP, PhD*

* Academic Unit of Respiratory Medicine, University of Sheffield, Sheffield, United Kingdom # Centre for Biomedical and Developmental Genetics, University of Sheffield, Sheffield, United Kingdom

CORRESPONDENCE: Stephen A. Renshaw, School of Medicine and Biomedical Sciences, University of Sheffield, Sheffield, UK


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Although we are separated from zebrafish by 160 million years of evolution, we share many features of the innate and adaptive immune systems. In addition, we can manipulate the genome of zebrafish, and observe the effects on inflammation in vivo as they are transparent in their larval stages. This has exciting implications for the study of inflammatory diseases.

We have established a model of inflammation in the zebrafish tail, in which caspase dependent cell death is required for resolution. For example, addition of the pan-caspase inhibitor zVD added at 4 hours after tailfin injury increases the number of neutrophils present from 6.0+/–1.0 to 28.9+/– 3.3 (mean +/– s.e.m. p<0.001 n = 3).

The transparency of the larvae makes these an ideal model for the study of in vivo inflammation, and we have generated fluorescent systems for the easy visualisation of neutrophilic inflammation and resolution in vivo.

We are also performing an unbiased forward genetic screen for mutants with defective resolution of inflammation, and to date have identified 38 putative mutants. These techniques allow new approaches to understanding the molecular controls of inflammation resolution.






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