Gene expression profile of endoscopically active and inactive ulcerative colitis: preliminary data

Vol. 58 No. 4, 2017

ROMANIAN JOURNAL of MORPHOLOGY and EMBRYOLOGY

Cristian George Tieranu, Maria Dobre, Teodora Ecaterina Manuc, Elena Milanesi, Iancu Emil Plesea, Caterina Popa, Mircea Manuc, Ioana Tieranu, Carmen Monica Preda, Mihai Mircea Diculescu, Elena Mirela Ionescu, Gabriel Becheanu

Aim: Multiple cytokines and chemokines related to immune response, apoptosis and inflammation have been identified as molecules implicated in ulcerative colitis (UC) pathogenesis. The aim of this study was to identify the differences at gene expression level of a panel of candidate genes in mucosa from patients with active UC (UCA), patients in remission (UCR), and normal controls. Patients, Materials and Methods: Eleven individuals were enrolled in the study: eight UC patients (four with active lesions, four with mucosal healing) and three controls without inflammatory bowel disease (IBD) seen on endoscopy. All the individuals underwent mucosal biopsy during colonoscopy. Gene expression profile was evaluated by polymerase chain reaction (PCR) array, investigating 84 genes implicated in apoptosis, inflammation, immune response, cellular adhesion, tissue remodeling and mucous secretion. Results: Seventeen and three genes out of 84 were found significantly differentially expressed in UCA and UCR compared to controls, respectively. In particular, REG1A and CHI3L1 genes reported an up-regulation in UCA with a fold difference above 200. In UCR patients, the levels of CASP1, LYZ and ISG15 were different compared to controls. However, since a significant up-regulation of both CASP1 and LYZ was observed also in the UCA group, only ISG15 levels remained associated to the remission state. Conclusions: ISG15, that plays a key role in the innate immune response, seemed to be specifically associated to the UC remission state. These preliminary data represent a starting point for defining the gene profile of UC in different stages in Romanian population. Identification of genes implicated in UC pathogenesis could be useful to select new therapeutic targets.

Corresponding author: Teodora Ecaterina Manuc, MD, PhD Candidate; e-mail: teodora.manuc@gmail.com

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