Title (srp)

Povezanost metaboličkog sindroma i imunskih parametara sa kliničkim i patohistološkim karakteristikama bolesnika sa ulceroznim kolitisom

Author

Jovanović, Marina, 1977-

Contributor

Zdravković, Nataša D., 1973-
Arsenijević, Nebojša, 1958-
Đukić, Aleksandar, 1967-
Đuranović, Srđan, 1965-

Description (srp)

Ulcerozni kolitis (engl. Ulcerative colitis- UC) je hronično oboljenje koje karakteriše zapaljenje sluznice digestivnog trakta, prvenstveno debelog creva. Metabolički sindrom je čest poremećaj značajno povezan sa UC. Veliki broj studija je pokazao značajan komorbiditet ovih poremećaja i njihovu genetsku povezanost. Cilj studije bio je da se ispita povezanost razvojnih faza metaboličkog sindroma sa težinom bolesti, te lokalnim i sistemskim imunskim odgovorom kod pacijenata sa ulceroznim kolitisom. Kod ispitanika sa ulceroznim kolitisom i metaboličkim sindromom zabeležena je klinički i patohistološki blaža bolest sa sistemskom i lokalnom predominacijom galektina 1, galektina 3 i imunosupresivnog citokina IL-10, uz sniženu koncentraciju proinflamacijskih citokina TNF-α, IL-6 i IL-17. Takođe je registrovana manja zastupljenost CD8+ T limfocita, a veća zastupljenost regulatornih CD4+Foxp3+ limfocita, kao i veća ekspresija galektina-3 na limfocitima i veća produkcija imunosupresivnog IL-10 u lamina propria-i obolelih od ulceroznog kolitisa sa metaboličkim sindromom. Kod ispitanika u terminalnoj fazi metaboličkog sindomoma zabeležena je klinički i patohistološki teža forma ulceroznog kolitisa. U ovoj grupi ispitanika nađena je sistemska i lokalna predominacija proinflamacijskih citokina TNF-α, IL-6 i IL-17 nad galektinom-1, galektina-3 nad proinflamacijskim medijatorima TNF-α i IL-17 kao i povećana ekspresija galektina-3 na imunokompetentnim ćelijama koje infiltrišu lamina propria-u. Lokalna i sistemska predominacija Gal-1 i Gal-3 nad proinflamacijskim citokinima kod obolelih sa metaboličkim sindromom može predstavljati mehanizam zaustavljanja i ograničavanja proinflamacijskog procesa i sprečiti oštećenje tkiva, ukazujući na imunosupresivnu ulogu Gal-1 i Gal-3 u biologiji ulceroznog kolitisa kod bolesnika sa metaboličkim sindromom. Sistemska i lokalna predominacija proinflamacijskih citokina TNF-α, IL-6 i IL-17 nad Gal-1 i Gal-3 u terminalnoj fazi metaboličkog sindroma pojačava zapaljenje i sledstveno oštećenje tkiva.

Description (eng)

Ulcerative colitis (UC) is a chronic disease characterized by inflammation of intestinal epithelium, primarily of the colon. Metabolic syndrome is a common disorder significantly associated with UC. A large number of studies have shown significant comorbidity of these disorders and their genetic linkage. The aim of the study was to examine the relationship between the developmental stages of the metabolic syndrome with the severity of the disease, and the local and systemic immune response in patients with ulcerative colitis. Clinical and pathohystologically mild disease with systemic and local prevalence of galectin 1, galectin 3 and immunosuppressive cytokine IL-10 was observed in subjects with ulcerative colitis and metabolic syndrome, with reduced concentration of proinflammatory cytokines TNF-α, IL-6, and IL-17. Further, we detected lower incidence of CD8+ T lymphocytes and enhanced accumulation of regulatory CD4+ Foxp3+ T cells, as well as increased expression of galectin-3 on lymphocytes and higher production of immunosuppressive IL-10 in lamina propria derived from UC patients with metabolic syndrome. Clinical and pathohystologically severe disease was observed in the patients with terminal phase of the metabolic syndrome. In this group of subjects, we found systemic and local prevalence of proinflammatory cytokines TNF-α, IL-6, and IL-17 over galectin-1; galectin-3 over TNF-α and IL-17; as well as increased expression of galectin-3 on immunocompetent cells infiltrating the lamina propria. Local and systemic dominance of Gal-1 and Gal-3 over proinflammatory cytokines in patients with metabolic syndrome may present a mechanism for stopping and limiting the proinflammatory process and preventing tissue damage, indicating the immunosuppressive role of Gal-1 and Gal-3 in the ulcerative colitis biology of patients with metabolic syndrome. Systemic and local prevalence of proinflammatory cytokines TNF-α, IL-6, and IL-17 over Gal-1 and Gal-3 in the terminal phase of the metabolic syndrome enhances inflammation and consequent tissue damage.

Object languages

Serbian

Date

2018

Rights

Creative Commons License
This work is licensed under a
CC BY-NC-ND 2.0 AT - Creative Commons Attribution - Non-Commercial - No Derivative Works 2.0 Austria License.

CC BY-NC-ND 2.0 AT

http://creativecommons.org/licenses/by-nc-nd/2.0/at/

Identifiers