title: The actin-bundling protein fascin is overexpressed in inflammatory bowel disease and may be important in tissue repair.
abstract: BACKGROUND
  Fascin is associated with increased cell motility in colorectal tumours but is absent from the normal colonic epithelium. We examined the expression of fascin in inflammatory bowel disease (IBD) and its location at regions undergoing restitution and regeneration. Tissue repair is essential for disease remission and we sought to determine the effects of therapeutic modalities on fascin expression and function using an in vitro model.
  
  
  METHODS
  Immunohistochemistry was performed on colonic tissue from IBD patients to determine changes in fascin expression and distribution. A human colorectal epithelial cell line was treated with 5-aminosalicylate (a common treatment for IBD), or sodium butyrate to determine the effect on fascin expression and cell motility.
  
  
  RESULTS
  Fascin overexpression was observed in both ulcerative colitis and Crohn's colitis and expression correlated with disease severity. Immunoreactivity was more intense and widespread in Crohn's compared to ulcerative colitis. Interestingly, highly expressing foci were consistently observed at the edges of ulcers where flattened, motile epithelial cells are actively involved in restitution, and also in areas of mucosal regeneration.5-aminosalicylate reduced fascin expression in colorectal epithelial cells and inhibited their motility. Conversely, sodium butyrate increased fascin expression and stimulated cell motility in the same cells.
  
  
  CONCLUSIONS
  Our data shows that fascin is overexpressed in inflammatory bowel disease and its location is indicative of a role in tissue repair. Our in vitro studies show that different therapeutic modalities may have converse effects on fascin expression and may have significant consequences for disease remission and the clinical management of IBD.
authors.affiliation: School of Cellular and Molecular Medicine, University of Bristol, UK. david.qualtrough@bristol.ac.uk
authors.forename: David
authors.initials: D
authors.lastname: Qualtrough
authors.forename: Katie
authors.initials: K
authors.lastname: Smallwood
authors.forename: David
authors.initials: D
authors.lastname: Littlejohns
authors.forename: Massimo
authors.initials: M
authors.lastname: Pignatelli
mesh_terms: D000199:Actins / Q000378:metabolism*; D000230:Adenocarcinoma / Q000473:pathology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002087:Butyrates / Q000494:pharmacology; D002352:Carrier Proteins / Q000378:metabolism*; D002460:Cell Line; D002465:Cell Movement / Q000187:drug effects; D003093:Colitis, Ulcerative / Q000378:metabolism / Q000503:physiopathology; D003106:Colon / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D003110:Colonic Neoplasms / Q000473:pathology; D003424:Crohn Disease / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000378:metabolism* / Q000503:physiopathology*; D019804:Mesalamine / Q000494:pharmacology; D008840:Microfilament Proteins / Q000378:metabolism*; D012038:Regeneration / Q000502:physiology*
chemical_list: D000199:Actins; D000894:Anti-Inflammatory Agents, Non-Steroidal; D002087:Butyrates; D002352:Carrier Proteins; D008840:Microfilament Proteins; C020324:fascin; D019804:Mesalamine