Laboratory research since 1985 has focused on the nature and consequences of altered mucosal glycosylation in gastro-intestinal disease. Recently this has included study of (i) bacteria-diet-epithelial interactions in pathogenesis of inflammatory bowel diseases (Crohn's disease and ulcerative colitis) and colorectal cancer; (ii) the role of the human galactose-binding lectin, galectin-3, in cancer metastasis and its inhibition by modified heparins. The altered mucosal glycosylation we found in inflammatory bowel disease and colon cancer led to studies co-led by Prof Barry Campbell (qv) investigating the mucosa-associated microbiota. Working with the late Prof Tony Hart (Med Microbiol) we found increased mucosa-associated E. coli in Crohn’s disease and colon cancer (Martin H et al Gastroenterology 2004;127:80-93). This complimented studies by Swidsinski et al and Darfeuille-Michaud et al , and since confirmed by many others. Collaboration with Christian Jobin showed that mucosal E. coli expressing the polyketide gene complex (pks) that leads to production of the genotoxin colibactin is associated with human sporadic colon cancer and also induces experimental inflammation-related colon cancer (Arthur JC et al Science 2012;338:120-3; Prorok-Hamon M et al Gut 2014;63:761-70). Further studies investigated interactions between mucosal E. coli and macrophages in Crohn’s disease (Mpofu et al, Gastroenterology 2007;133:1487-98; Subramanian S et al Antimicrob Agents Chemother 2008;52:427-34; Flanagan P et al IBDJ Dis 2015;21:1499-510).