Abstract
We read with great interest the excellent work of Vasudeva et al., 2015 Vasudeva K. Vodovotz Y. Azhar N. Barclay D. Janjic J.M. Pollock J.A. In vivo and systems biology studies implicate IL-18 as a central mediator in chronic pain. J. Neuroimmunol. 2015; 283: 43-49 Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar who investigated the role of cytokines and chemokines in a rat chronic constriction injury model. In vivo investigation and Dynamic Bayesian Network modelling identified interleukin-18 (IL-18) as a central node associated with neuropathic pain, and interferon gamma (IFN-γ) and interleukin-1 beta (IL-1β) as central nodes associated with tissue injury. We believe this to be a significant finding, adding to the body of evidence that has identified IL-18 as a central mediator of chronic inflammation ( Bombardieri et al., 2007 Bombardieri M. McInnes I.B. Pitzalis C. Interleukin-18 as a potential therapeutic target in chronic autoimmune/inflammatory conditions. Expert. Opin. Biol. Ther. 2007; 7: 31-40 Crossref PubMed Scopus (28) Google Scholar ). Their findings have revealed IL-18 as a central node in the maintenance of neuropathic pain, and hence, a potential therapeutic target for the prevention of chronic neuropathic pain post-injury.
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