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Circulating fibrocytes and Crohn’s disease. BJS 2013; 100: 1549-1556.

Published: 9th October 2013

Authors: S. M. Sahebally, J. P. Burke, K. H. Chang, M. G. Kiernan, P. R. O'Connell, J. C. Coffey et al.


Despite 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.


The electronic literature (January 1972 to December 2012) on ‘circulating fibrocytes’ and ‘Crohn's fibrosis’ was reviewed.


Circulating 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.


Levels 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.

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