Comment

Rats given an intracolonic injection of the contact sensitising agent trinitrobenzene sulphonic (TNBS) acid dissolved in ethanol develop transmural inflammation resembling Crohn’s disease. Although the model has limitations, the advantage of the system is that it allows pre-clinical studies on possible treatments to be easily carried out, and it is a much easier system to work with than the spontaneous models of inflammatory bowel disease (IBD) which occur in gene knockout mice. Tissue injury in this model is T cell mediated, and the response is against both the hapten and the normal flora. The T cell response is highly skewed towards Th1 and there is abundant interferon (IFN) γ and tumour necrosis factor (TNF) α in the mucosa, again like Crohn’s disease. As it is now well established that Th1 responses can be dramatically down-regulated by Th2 cytokines such as interleukin (IL) 4 and IL-10, Hogaboam et al have attempted to find out whether IL-4 prevents TNBS colitis in rats. Raised IL-4 concentrations can be achieved in vivo by direct injection of recombinant protein, but in this work the authors have used a recombinant human adenovirus 5 vector expressing murine IL-4. The virus was given intraperitoneally and infected cells in the liver, diaphragm, and after two injections, the colon. IL-4 serum concentrations were elevated. The bottom line …