Convincing evidence from both animal models and the study of patients with ulcerative colitis (UC) implicates the intestinal microflora in the initiation and maintenance of the inflammatory processes in this condition. Despite this, no specific pathogen has been identified as causal and the disease is widely believed to occur as the result of a genetically determined, but abnormal immune response to commensal bacteria. When compared with healthy people, UC patients have increased levels of mucosal IgG directed against the normal microflora. Studies of mucosal bacterial populations in UC indicate that there may be increased numbers of organisms, but reduced counts of "protective" bacteria such as lactobacilli and bifidobacteria. In animal models of colitis, antibiotics, particularly metronidazole, clindamycin, ciprofloxacin and the combination of vancomycin/impinemem protect against UC, especially if given before the onset of inflammation. These antibiotics target anaerobes and some Gram-positive organisms such as enterococci. However, antibiotic use in more than a dozen randomised control trials has been very disappointing, probably because we do not know which species to target, when to give the antibiotics, for how long and in what combinations. Surprisingly, therefore, there is a consistent benefit in the small number of studies reported of probiotics to manage UC and pouchitis. There is scope for more work in this area focussing on the mucosal microflora, its interactions with the gut immune system, its metabolic properties and the potential ways of modifying it.