Author:
Davydova E. V.,Osikov M. V.,Bakeeva A. E.,Kaigorodtseva N. V.
Abstract
Worldwide incidence of digestive system disorders doubles each decade, thus representing a significant medical and social problem. Despite lacking knowledge in pathogenesis of inflammatory bowel diseases, it is clear that serum cytokine imbalance, and lesions in the walls of gastrointestinal tract are observed in experimental colitis. Pathogenesis of UC remains controversial due to a large set of etiological factors that initiate activation of cellular and humoral mechanisms of the immune response upon development of inflammatory changes in the large intestine. At the same time, cytokine secretion and expression have not been studied in details. The aim of the work was to study the cytokine profile of blood in rats using the experimental oxazolone model of ulcerative colitis. The work was performed in 40 white Wistar rats; ulcerative colitis was induced by rectal administration of a 3% alcohol solution of oxazolone. For anesthesia, Zoletil-100 (INN: tiletamine hydrochloride, VirbacSanteAnimale; France) was used at a dose of 20 mg/kg. The studies were carried out on the 2nd, 4th and 6th days. Serum concentration of IL-6, IL-8, IL-17 and IL-23 was determined by means of automatic ELISA analyzer “Personal LAB” using a specific test system for rats. For immunohistochemistry of Treg cells, we used anti-FoxP3 antibody (Arigo Biolaboratories, Тайвань) followed by immunhistostaining in VENTANA BenchMark XT (USA). Statistical evaluation was performed by non-parametric Mann-Whitney and Wald-Wolfowitz criteria. The difference was considered significant at р ≤ 0.05. In rats with experimental colitis, an increase of proinflammatory IL-17 which acts by attraction of neutrophils and other cells of innate immunity, supporting chronic inflammation and autoimmune reactions. We have found an increase of serum IL-23 concentration in rats with experimental ulcerative colitis on days 2, 4 and 6 of the experiment. This cytokine induces and maintains the inflammatory process in the wall of the large intestine. Significant decrease of FoxP3+Т-lymphocytes was revealed in colonic tissues, thus suggesting appropriate local autoimmune disorders.
Subject
Immunology,General Medicine
Reference15 articles.
1. Долгушина А.И., Хусаинова Г.М., Василенко Г.М., Кононенко А.Г. Распространенность воспалительных заболеваний кишечника в Челябинской области // Альманах клинической медицины, 2019. Т. 47, № 6. С. 511-517.
2. Дьяченко П.А., Дьяченко А.Г. Клетки Th17 и их роль в возникновении аутоиммунных заболеваний // 1мунолопя та алерголопя: наука i практика, 2011. № 2. С. 4-10.
3. Bo L., Fu H., Yang J. Comprehensive analysis of gene expression profiles provides insight into the pathogenesis of Crohn's disease. Mol. Med. Rep., 2018, Vol.18, no. 3, pp. 2643-2650.
4. Relationship between the IL23R SNPs and Crohn’s Disease Susceptibility and Phenotype in the Polish and Bosnian Populations: A Case-Control Study
5. Burisch J., Munkholm P. The epidemiology of inflammatory bowel disease. Scand. J. Gastroenterol., 2015, Vol. 50, no. 8, pp. 942-951.