In response to stress and damage, cells secrete ATP, stimulating pro-inflammatory mediators through purinergic receptor activation.[37] Increased ATP release from human intestinal epithelial cells and human urothelial cells has been linked to cell death within the context of inflammatory gut and bladder disease, respectively.[35,38] Similarly, increased levels of the pro-inflammatory cytokines IL-6 and IL-8 have been demonstrated from airway cells after stimulation by bacteria,[39] viral infection,[40] and in nasal epithelial cells after challenge with an antigen.[41]. This evidence concerns the gene CXCL8 and viral infectious disease.