Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/8595
Title: TGF-Β as a Marker of Ulcerative Colitis and Disease Severity
Authors: Jovanovic M.
Zdravković N.
Jovanovic I.
Radosavljevic, Gordana
Gajovic N.
Zdravković N.
Maric V.
Arsenijevic, Nebojsa
Issue Date: 2018
Abstract: © 2017 Marina Jovanovic et al., published by De Gruyter Open 2017. Ulcerative colitis (UC) represents chronic inflammation of the large intestine. Immune response plays an important role in disease genesis and progression. Activated leukocytes secrete several cytokines that actively regulate the inflammatory response in UC. The aim of this study was to determine levels of cytokines IL-17, IL-27, IFN-γ and TGF-β in patients with UC and to test them as biomarkers for disease. The blood samples of 24 patients with ulcerative colitis without previous treatment and 37 healthy individuals were analyzed. Serum levels of IL-17, IL-27, IFN-γ and TGF-β were measured using sensitive enzyme-linked immunosorbent assay (ELISA) kits. Serum levels of IL-17, IL-27, IFN-γ and TGF-β were increased in patients with UC, compared to healthy controls (p=0.022; p=0.001; p=0.001; and p=0.002; respectively). Ratios of cytokines IL-27/IL-17, IFN-γ /TGF-β and IL-17/TGF-β were significantly higher in group of patients with UC (p=0.002; p=0.002; p=0.003; respectively). Serum value of TGF-β higher than 20 pg/ml presents a highly sensitive and specific marker for UC. We believe that increased production and predominance of immunosupressive TGF-β may represent compensatory mechanism for ongoing pro-inflammatory processes in UC.
URI: https://scidar.kg.ac.rs/handle/123456789/8595
DOI: 10.1515/sjecr-2017-0019
ISSN: 1820-8665
SCOPUS: 2-s2.0-85042735121
Appears in Collections:Faculty of Medical Sciences, Kragujevac

Page views(s)

512

Downloads(s)

20

Files in This Item:
File Description SizeFormat 
10.1515-sjecr-2017-0019.pdf1.34 MBAdobe PDFThumbnail
View/Open


This item is licensed under a Creative Commons License Creative Commons