Associations Between Metabolic Syndrome, Ulcerative Colitis, and Fecal sST2 and CXCL8 Levels: Unveiling New Inflammatory Pathways

Author:

Vucelj Samir1,Corovic Irfan1,Jovanovic Marina2,Petrovic Andjela3,Stanisavljevic Isidora3,Stojanovic Bojan4,Corovic Kemal5,Andrejevic Ivana6,Zdravkovic Natasa2,Stojanovic Milica Dimitrijevic7,Balovic Goran4,Stojanovic Bojana6

Affiliation:

1. General Hospital “Novi Pazar” , Novi Pazar , Serbia , Department of Gastroenterohepatology

2. University of Kragujevac, Faculty of Medical Sciences , Department of Internal medicine , Serbia

3. University of Kragujevac, Faculty of Medical Sciences , Center for Molecular Medicine and Stem Cell Research , Serbia

4. University of Kragujevac, Faculty of Medical Sciences , Department of Surgery , Serbia

5. Health Center Tutin , Serbia

6. University of Kragujevac, Faculty of Medical Sciences , Department of Pathophysiology , Serbia

7. University of Kragujevac, Faculty of Medical Sciences , Department of Pathology , Serbia

Abstract

Abstract Ulcerative Colitis (UC), a chronic inflammatory bowel disease, exhibits complex interactions with metabolic disorders such as Metabolic Syndrome (MetS), which can significantly impact disease progression and patient outcomes. Among the multitude of players in this intricate network, soluble ST2 (sST2) and Chemokine (C-X-C motif) ligand 8 (CXCL8) have emerged as critical mediators of immune responses, potentially modulating the disease course in UC patients with co-existing MetS. This study aimed to investigate the association between Metabolic Syndrome (MetS) and immune response modulation in patients with Ulcerative Colitis (UC). UC patients, stratified by the presence of MetS, underwent clinical, endoscopic, and histological evaluation, along with blood and fecal biochemical analyses. Serum and fecal concentrations of sST2 and CXCL8 were measured and compared between groups. UC patients with MetS exhibited lower white blood cell (WBC) count, higher levels of metabolic markers, and milder disease severity on clinical, endoscopic, and histological scales. Serum concentrations of sST2 and CXCL8 were similar between UC patients with and without MetS. However, fecal levels of these cytokines were significantly elevated in UC patients with MetS, suggesting a localized intensified immune response. Our findings indicate a potential dichotomy in the immune response of UC patients with MetS, characterized by a dampened systemic inflammation and heightened local immune response. The elevated fecal levels of sST2 and CXCL8 underscore a potentially unique immune modulation within the gut in the presence of MetS. These findings shed new light on the pathophysiological interplay between MetS and UC and may provide new avenues for targeted therapeutic strategies.

Publisher

Walter de Gruyter GmbH

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