4.4 Article

Mucosal gene expression profile of stricturing Crohn's disease: A preliminary study

Journal

EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 23, Issue 2, Pages -

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2021.11072

Keywords

strictures; Crohn's disease; genes; formyl-peptide receptor 1; IFN-gamma-inducible protein 10; C-C chemokine ligand 25; C-C chemokine receptor type 1

Funding

  1. Ministry of Education and Research in Romania [7PFE/16.10.2018, PN 1N/2019_19.29.01.05]

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This study identified four genes with significantly increased expression in the mucosa of patients with stricturing Crohn's disease compared to those with inflammatory Crohn's disease. These findings may help elucidate the mechanisms leading to disease-associated complications.
Intestinal strictures are an important complication of Crohn's disease (CD), with similar to 40% of patients developing symptomatic obstruction within 10 years of diagnosis. However, there is a paucity of research examining the mechanisms driving the development of fibrotic strictures in CD. The present study aimed to identify the mucosal markers associated with stricturing complications by examining the differences in the gene expression profiles of two patient cohorts: Patients diagnosed with inflammatory CD (n=12) and patients with stricturing CD (n=9). For each patient, a paired sample of inflamed and uninflamed mucosa was isolated and assessed by quantitative PCR using a large panel of genes associated with inflammatory bowel disease. The presents study revealed a significantly increased level of four genes in the mucosa of patients with strictures compared with the inflammatory pattern of the disease: Formyl-peptide receptor 1 [P=0.019; fold change (FC)=11.6], C-C chemokine receptor type 1 (P=0.035; FC=5.44), IFN-gamma-inducible protein 10 (P=0.037; FC=3.8) and C-C chemokine ligand 25 (P=0.048; FC=3.56). The augmented expression of these four genes in the CD stricturing phenotype, if confirmed in larger cohorts of patients, could help elucidate the mechanisms leading to disease-associated complications.

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