Circulating fibrocytes and Crohn's disease

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

Research output: Contribution to journalReview articlepeer-review

Abstract

Background 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. Methods The electronic literature (January 1972 to December 2012) on 'circulating fibrocytes' and 'Crohn's fibrosis' was reviewed. Results 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. Conclusion 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. Fibrocytes as the key to Crohn's disease

Original languageEnglish
Pages (from-to)1549-1556
Number of pages8
JournalBritish Journal of Surgery
Volume100
Issue number12
DOIs
Publication statusPublished - Nov 2013
Externally publishedYes

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