In this issue, Kolios et al. have presented a paper on how the fluoroquinolone ciprofloxacin inhibits cytokine-induced nitric oxide (NO) production in human colonic epithelium [1]. The HT-29 colonic epithelial cell-line and colonic biopsies from patients suffering ulcerative colitis were stimulated with a mixture of interleukin (IL)-1α, tumour necrosis factor (TNF)-α and interferon (IFN)-γ in the presence of ciprofloxacin. The cytokine-dependent induction of NO synthase mRNA was found to be inhibited by the quinolone. As wortmannin counteracted the ciprofloxacin-dependent inhibition, a possible interaction of ciprofloxacin with the phosphatidylinositol (PI)-3 kinase pathway was suggested. The clinical implications of this present paper are that treatment of ulcerative colitis with ciprofloxacin may be beneficial during exacerbations in order to decrease the inflammatory response.

During the past two decades increased interest has been shown in the immunodulatory activities of antibacterial agents and in particular with putative effects in immunocompromised hosts. The effects of antibiotics on human cells have been described for most antibiotics that accumulate intracellularly. Quinolones, macrolides and latterly tetracyclines have been extensively studied [2–6]. Mostly, the inhibitory effects of these agents are suggested to be beneficial, although a few examples of stimulatory actions have also been described, particularly for the quinolones. Other antibacterial agents such as rifampin, fusidic acid and nitrofurantoin also interfere with the human host in certain experimental systems [3], but these will not be discussed in this context.