A galectin-specific signature in the gut delineates Crohn?s disease and ulcerative colitis from other human inflammatory intestinal disorders

PAPA GOBBI R; DE FRANCESCO N; BONDAR C; MUGLIA C; CHIRDO F.G; RUMBO, M; ROCCA A; TOSCANO M; SAMBUELLI A; RABINOVICH G; DOCENA G

BIOFACTORS

IOS PRESS

Lugar: Amsterdam; Año: 2016 vol. 42 p. 93 - 105

0951-6433

Inflammatory bowel diseases (IBD) are idiopathic, chronic and relapsing inflammatory conditions of the gastrointestinal tract. Galectins, a family of animal lectins defined by shared consensus amino acid sequence and affinity for β-galactosides containing oligosaccharides, are polyfunctional proteins in a wide range of biological processes, and its role in IBD has not been completely explored. In this work we analyzed the expression of Galectin (Gal)-1, Gal-3, Gal-4 and Gal-9 in intestinal biopsies, and proposed an integrated analysis of the expression of these four galectins as novel mucosal markers for IBD. Colonic biopsies were obtained in 73 IBD patients (24 Crohn´s disease-CD, and 49 ulcerative colitis-UC), 9 patients with rejection after gut transplantation, 8 adult patients with celiac disease and 32 non-IBD donors. The study of galectin expression was performed by mRNA isolation, RT-PCR and qPCR using specific primers for individual galectins and β-actin. A linear discriminant analysis (LDA) was used to analyze the expression of the four galectins in individual biological samples.We found that galectin expression was dysregulated and showed a specific profile in inflamed tissues from IBD, whereas non-inflamed IBD or control samples shared the same pattern expression. LDA could discern between different inflammation grades in active areas of IBD, and showed that remission IBD samples were clusterized with control samples. CD was not distinguished from UC, even with the addition of transcription factors that have been associated to IBD. Furthermore, inflamed IBD was discriminated from inflamed tissue of rejected gut in transplanted patients and duodenum of celiac patients, which were not discriminated from control duodenum samples.