Progress does not just come in giant leaps: adapting techniques for the study of inflammation to novel applications
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Discussion of the relevance of suitable experimental models for the effective translation of drug effects to clinical inflammatory diseases has a long history. Much emphasis is placed these days on genetically transformed mice, which may have developmental drawbacks. But are established models redundant?
Drawn from personal experience, examples are provided of the success of tinkering with technology in the context of inflammation. These include the use of specific dietary deficiency conditions, the development of new applications for established drugs and the introduction of a variety of readouts to assess outcome in studies on established disease models. Such approaches have been used to demonstrate inflammation-modulating effects of prostaglandin E, in the development of ebselen, for the introduction of immunomodulatory macrolide drugs and in new approaches to the therapy of multiple sclerosis.
Fine tuning of experimental approaches and evaluation technologies can often still provide innovative, clinically relevant insights into the potential beneficial effects of drugs and pharmacological agents.
KeywordsModels of inflammation Drug effects Ebselen Prostaglandin E Azithromycin EAE
Whatever research project is being pursued, people with high quality technical skills are crucial. I have been fortunate to work in research teams with many such people, some of whom I have cited in this article and for whose collaboration and friendship I am most grateful. Perhaps one of my main contributions to the teams was my ability to give clear presentations and to write in my native language, having spent most of my research career in non-English-speaking countries! I also wish to thank various members of committees of the International Association of Inflammation Societies (IAIS) and the Inflammation Research Association (IRA) in the US with whom I have worked over the years and developed good friendships and the latest IAIS committee for the Lifetime Achievement Award. I am delighted to share the award with Ian Ahnfelt-Rønne, a long-standing colleague and friend, mindful of the many years we shared editing Inflammation Research and for the productive co-operation with Detlef-Klueber at Springer. I also thank the LOEWE Research Center for Translational Medicine and Pharmacology of the State of Hesse for financial support of the work in Frankfurt.
- 28.Bonta IL. Essential fatty acid deficient animals as tools for the study of some cardiovascular and related functions. Acta Cardiol Suppl. 1979:62–6.Google Scholar
- 34.Zhang YY, Desai A, Yang SY, Bae KB, Antczak MI, Fink SP, et al. Inhibition of the prostaglandin-degrading enzyme 15-PGDH potentiates tissue regeneration. Science. 2015;348:1223.Google Scholar
- 68.Bosnar M, Bosnjak B, Cuzic S, Hrvacic B, Marjanovic N, Glojnaric I, et al. Azithromycin and clarithromycin inhibit lipopolysaccharide-induced murine pulmonary neutrophilia mainly through effects on macrophage-derived granulocyte-macrophage colony-stimulating factor and interleukin-1beta. J Pharmacol Exp Therap. 2009;331:104–13.CrossRefGoogle Scholar
- 71.Bosnar M, Cuzic S, Bosnjak B, Nujic K, Ergovic G, Marjanovic N, et al. Azithromycin inhibits macrophage interleukin-1beta production through inhibition of activator protein-1 in lipopolysaccharide-induced murine pulmonary neutrophilia. Int Immunopharmacol. 2011;11:424–34.CrossRefPubMedGoogle Scholar
- 92.Finn CA. Artifacts: An Archaeologist's Year in Silicon Valley 2001. MIT Press, Cambridge, MA, p. 90Google Scholar
- 93.Szent-Gyorgyi A. BrainyQuote.com, Xplore Inc, 2016. http://www.brainyquote.com/quotes/quotes/a/albertszen389956.html. Accessed 20 Sep 2016