Review Sulphate-reducing bacteria and hydrogen sulphide in the aetiology of ulcerative colitis F. E. Rowan 1,2 , N. G. Docherty 1,2 , J. C. Coffey 2,3 and P. R. O’Connell 1,2,3 1 School of Medicine and Medical Sciences and 2 Conway Institute of Biomolecular and Biomedical Research, University College Dublin, and 3 Surgical Professorial Unit, St Vincent’s University Hospital, Dublin, Ireland Correspondence to: Professor P. R. O’Connell, Surgical Professorial Unit, St Vincent’s University Hospital, Dublin 4, Ireland (e-mail: Ronan.OConnell@ucd.ie) Background: The aetiology of ulcerative colitis is uncertain but may relate to environmental factors in genetically predisposed individuals. Sulphate-reducing bacteria (SRB) have been implicated through the harmful effects of hydrogen sulphide, a by-product of their respiration. Hydrogen sulphide is freely permeable to cell membranes and inhibits butyrate. This review examines the available evidence relating to SRB as a possible cause of ulcerative colitis. Methods: A literature search was conducted using the PubMed database and search terms ‘sulphate reducing bacteria’, ‘hydrogen sulphide’, ‘ulcerative colitis’, ‘mucous gel layer’ and ‘trans-sulphuration’. Results: Search results were scrutinized and 113 pertinent full-text articles were selected for review. Collected data related to hydrogen sulphide metabolism, SRB respiration, mucous gel layer composition and their association with ulcerative colitis. Conclusion: There is evidence to implicate SRB as an environmental factor in ulcerative colitis. More sophisticated mucosal dissection and molecular techniques using bacteria-directed probes are required to determine an association definitively. Paper accepted 7 October 2008 Published online in Wiley InterScience (www.bjs.co.uk). DOI: 10.1002/bjs.6454 Introduction Ulcerative colitis may occur in genetically predisposed individuals whose immune system cannot respond appro- priately to changes in bowel flora 1 . Sulphate-reducing bacteria (SRB) are obligate anaerobic flagellated bacteria that contribute to the interaction between colonic flora and epithelium. Faecal carriage of active SRB, as measured in faecal slurry, is greater in patients with ulcerative colitis than in healthy controls 2 . Cultures obtained from mucosal biopsies have not shown such clear differences 3 , but SRB have been shown preferentially to colonize ileal pouches in patients with a background of ulcerative colitis compared with those with familial adenomatous polyposis 4 . New lab- oratory techniques, particularly use of 16S ribosomal RNA probes, accurately determine SRB colonization and permit further exploration of the potential association between SRB and ulcerative colitis 5 . Hydrogen sulphide is the principal by-product of SRB metabolism. It is produced endogenously by colonocytes by a process known as trans-sulphuration. Hydrogen sulphide at non-toxic concentrations is physiologically active in the brain, heart, vasculature, urogenital system and gastrointestinal tract 6,7 . At higher concentrations, it inhibits butyrate oxidation, the principal energy source for colonocytes 8 . Hydrogen sulphide has been implicated in ulcerative colitis 9 ; it is increased in the faeces of patients with ulcerative colitis 10 . A unifying continuum may exist with SRB exerting a harmful effect on colonocytes through their contribution to a greater than physiological volume of hydrogen sulphide in the colonic lumen of patients with ulcerative colitis. The aim of this review is to draw together available evidence relating SRB to the aetiology of ulcerative colitis. Specific concepts are addressed: endogenous production and clearance of hydrogen sulphide, the effects of hydrogen sulphide on cellular integrity, SRB production of hydrogen sulphide, SRB carriage in ulcerative colitis, and SRB colonization of the mucous gel layer. Copyright  2009 British Journal of Surgery Society Ltd British Journal of Surgery 2009; 96: 151–158 Published by John Wiley & Sons Ltd