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World J Gastrointest Pathophysiol. Aug 15, 2013; 4(3): 53-58
Published online Aug 15, 2013. doi: 10.4291/wjgp.v4.i3.53
Published online Aug 15, 2013. doi: 10.4291/wjgp.v4.i3.53
Altered molecular pattern of mucosal healing in Crohn’s disease fibrotic stenosis
Enzo Ierardi, Floriana Giorgio, Santina Cantatore, Michele Barone, Carmine Panella, Gastroenterology, Department of Medical and Surgical Sciences, University of Foggia, 71100 Foggia, Italy
Domenico Piscitelli, Mariabeatrice Principi, Maria Grazia Fiore, Roberta Rossi, Alfredo Di Leo, Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, Italy
Author contributions: Ierardi E, Barone M, Di Leo A and Panella C designed the study, revised the manuscript and approved the final version; Giorgio F, Piscitelli D, Principi M, Fiore MG and Rossi R collected the data; Cantatore S performed immunohistochemistry.
Correspondence to: Enzo Ierardi, Professor, Gsatroenterology, Department of Medical and Surgical Sciences, University of Foggia, AOU Ospedali Riuniti, Viale Pinto, 71100 Foggia, Italy. enzo.ierardi@fastwenet.it
Telephone: +39-8-81736204 Fax: +39-8-81733848
Received: April 6, 2013
Revised: June 17, 2013
Accepted: July 18, 2013
Published online: August 15, 2013
Processing time: 117 Days and 10.4 Hours
Revised: June 17, 2013
Accepted: July 18, 2013
Published online: August 15, 2013
Processing time: 117 Days and 10.4 Hours
Core Tip
Core tip: The present manuscript reports a study of molecular pattern in the course of stenotic complication of Crohn’s disease. We have studied the interaction among the main cytokine [tumor necrosis factor-α (TNF-α)], an adhesion molecule (syndecan 1) and a growth factor basic fibroblast growth factor which are strictly involved in damage repair and mucosal healing, as showed in a previous study. In this study we demonstrated that a deep dysregulation of interaction of these three factors may support stenotic fibrosis in Crohn’s disease and suggest that this condition needs to be investigated before a biological treatment since TNF-α lack downregulation could further stimulate fibrogenesis.