• S M Sahebally, J P Burke, K H Chang, M G Kiernan, P R O'Connell, and J C Coffey.
• Department of Colorectal Surgery, University Hospital Limerick; and 4i Centre for Interventions In Inflammation, Infection and Immunity, Graduate Entry Medical School, University of Limerick, Limerick.
• Br J Surg. 2013 Nov 1;100(12):1549-56.

BackgroundDespite advances in medical therapy, there remains no effective preventive or non-surgical therapeutic option for fibrostenotic Crohn's disease (CD). Symptomatic recurrences are common, necessitating reintervention. Intestinal fibroblasts mediate stricture formation, but their exact source is unclear. Recent evidence indicates that circulating fibrocytes drive fibrosis through differentiation into fibroblasts and the production of extracellular matrix proteins. The aim of this review is to describe current understanding of the pathophysiology underlying fibrosis in CD, the cellular and molecular biology of fibrocytes and their role in CD.MethodsThe electronic literature (January 1972 to December 2012) on 'circulating fibrocytes' and 'Crohn's fibrosis' was reviewed.ResultsCirculating fibrocytes appear universally involved in organ fibrosis. A complex array of cytokines, chemokines and growth factors regulate fibrocyte biology, and these are associated with fibrogenesis in CD. The cytokines transforming growth factor β1, connective tissue growth factor and interleukin 13, overexpressed in the strictured Crohn's intestine, promote fibrocyte generation and/or differentiation.ConclusionLevels of circulating fibrocytes are raised in conditions marked by exaggerated fibrosis. These and other observations prompt a characterization of fibrocyte activity in CD with a view to investigating a pathogenic role.© 2013 British Journal of Surgery Society Ltd. Published by John Wiley & Sons Ltd.

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