The bladder irritation that results from Foley catheterization appears to be mediated by muscarinic receptors that mediate involuntary bladder smooth-muscle contractility. Thus the main therapy relies on agents with anti-muscarinic activity such as oxybutynin, tolterodine and butylscopolamine, whereas some benefit has been shown with tramadol, ketamine, paracetamol, pregabalin and gabapentin. However no single commonly accepted therapy for FCRBD is available, and there is uncertainty about the safety and efficacy of the current treatments available. Some research has suggested a role for inflammatory mediators in the occurrence of FCRBD as evident by induction of prostaglandin synthesis and cyclooxygenase-2 (COX-2) inhibitors alleviating symptoms related to FCRBD. In summary various therapies to control FCRBD are available but none have directly addressed the acute inflammatory reaction likely mediating these symptoms1,2,3,4. Hence our interest in analyzing the activity of acute inflammatory cells in particular neutrophil activation as a mediator of bladder inflammation and trigger of FCRBD.