PhD Scientific Days 2017

Oral Presentations: Head&Neck & Basic Sciences I.

The role of the interleukin-24 in the pathomechanism of IBD-associated tissue remodelling

Előadó neve

Dr. Veres-Székely, Apor, PhD

Előadó munkahelye

Semmelweis University, 1st Dept. of Pediatrics

Előadó telefonszáma

+36304960831

Előadó e-mail címe

veres.sz.apor@gmail.com

Az előadás címe

The role of the interleukin-24 in the pathomechanism of IBD-associated tissue remodelling

Szerző(k) neve és munkahelye

Apor Veres-Székely1,2, Anna Ónody2, Erna Sziksz1,2, Domonkos Pap1,2, Réka Rokonay2, Rita Lippai2, István M. Takács2, Attila J. Szabó1,2, Ádám Vannay1,2

1 MTA-SE, Pediatrics and Nephrology Research Group, Budapest, Hungary
2 1st Dept. of Pediatrics, Semmelweis University, Budapest, Hungary

Szekció

Oral Presentations: Head&Neck & Basic Sciences I.

Data of the presenter

Doctoral School: Doctoral School of Clinical Medicine
Program: Prevention of Chronic Diseases in Childhood
Supervisor: Ádám Vannay
E-mail: veres.sz.apor@gmail.com, veres-szekely.apor@med.semmelweis-univ.hu

Text of the abstract

Introduction: Interleukin(IL)-24 is a member of IL-20 cytokine subfamily which immunomodulatory effect is well known. The aim of our study was to investigate the role of IL-24 in the pathomechanism of inflammatory bowel disease (IBD) and determine its effect in the disease-associated tissue remodeling.
Methods: Localization and expression of IL-24 and their receptor (IL-20RB) were investigated in the colonic biopsy samples of children with IBD and controls (n=16/groups) by immunofluorescent staining or real time RT-PCR, respectively. Serum IL-24 levels in the two groups were determined by ELISA method. Effect of IL-24 on the expression of fibrosis-related genes was investigated by RT-PCR, Western-blot, and flow cytometry in the experimental model of IBD induced by dextran sodium sulphate (DSS) in wild type C57B6 and IL-20RB knock out (KO) mice (n=6/groups), and in colonic epithelial and fibroblast cell lines.
Results: We found elevated IL-24 expression in the inflamed colonic mucosa and serum of children with IBD compared to controls. IL-24 increased the expression of profibrotic genes (TGF-ß, PDGF-B) in colonic epithelial cells and of fibrosis associated genes (COL1, COL3, FN1, MMP2,-9, TIMP1,-2) in fibroblast cells as well. DSS treatment induced the IL-24 expression in the colonic mucosa of wild type mice. Lack of IL-20RB in the KO mice resulted in decreased expression of fibrosis-related genes (TGF-ß, PDGF-B, COL1, COL3, FN1, MMP2, TIMP2) after colitis induction by DSS.
Discussion: IL-24 may promote tissue remodeling shifted toward an excessive deposition of extracellular matrix components directly by acting on fibroblast and indirectly via induction of pro-fibrotic factors on epithelial cells. Our data suggest that inhibition of IL-24 may have a significant anti-fibrotic effect, thus it could serve as potential target molecule in the therapy of IBD.

Grant support: OTKA PD105361, -K108688, -K116928, LP2011-008

Kind

Szabad

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

1245

Authors (legacy)

Apor Veres-Székely1,2, Anna Ónody2, Erna Sziksz1,2, Domonkos Pap1,2, Réka Rokonay2, Rita Lippai2, István M. Takács2, Attila J. Szabó1,2, Ádám Vannay1,2

1 MTA-SE, Pediatrics and Nephrology Research Group, Budapest, Hungary
2 1st Dept. of Pediatrics, Semmelweis University, Budapest, Hungary