代谢综合征、溃疡性结肠炎与粪便 sST2 和 CXCL8 水平之间的关系:揭示新的炎症途径

Samir Vucelj, Irfan Corovic, Marina Z Jovanovic, Andjela Petrović, Isidora Stanisavljević, Bojan Stojanović, Kemal Corovic, Ivana Andrejevic, N. Zdravković, Milica Dimitrijevic Stojanovic, Goran Balovic, Bojan Stojanović
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摘要

溃疡性结肠炎(UC)是一种慢性炎症性肠病,与代谢综合征(Metabolic Syndrome,MetS)等代谢性疾病之间存在复杂的相互作用,会对疾病的进展和患者的预后产生重大影响。在这一错综复杂网络的众多参与者中,可溶性 ST2(sST2)和趋化因子(C-X-C motif)配体 8(CXCL8)已成为免疫反应的关键介质,有可能调节合并 MetS 的 UC 患者的病程。本研究旨在探讨代谢综合征(MetS)与溃疡性结肠炎(UC)患者免疫反应调节之间的关联。根据 MetS 的存在情况对 UC 患者进行了临床、内窥镜和组织学评估,以及血液和粪便生化分析。对血清和粪便中的 sST2 和 CXCL8 浓度进行了测量,并在各组之间进行了比较。患有 MetS 的 UC 患者白细胞(WBC)计数较低,代谢标记物水平较高,临床、内窥镜和组织学评分的疾病严重程度较轻。患有和未患有 MetS 的 UC 患者血清中的 sST2 和 CXCL8 浓度相似。然而,有 MetS 的 UC 患者粪便中这些细胞因子的水平明显升高,表明局部免疫反应增强。我们的研究结果表明,患有 MetS 的 UC 患者的免疫反应可能存在两极分化,其特点是全身炎症反应减弱,而局部免疫反应增强。粪便中 sST2 和 CXCL8 水平的升高强调了 MetS 存在时肠道内潜在的独特免疫调节。这些发现为 MetS 和 UC 之间的病理生理学相互作用提供了新的线索,并可能为靶向治疗策略提供新的途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Associations Between Metabolic Syndrome, Ulcerative Colitis, and Fecal sST2 and CXCL8 Levels: Unveiling New Inflammatory Pathways
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.
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