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Chemokine and cytokine levels in inflammatory bowel disease patients

机译：炎症性肠病患者的趋化因子和细胞因子水平

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Crohn's disease (CD) and ulcerative colitis (UC), two forms of inflammatory bowel disease (IBD), are chronic, relapsing, and tissue destructive lesions that are accompanied by the uncontrolled activation of effector immune cells in the mucosa. Recent estimates indicate that there are 1.3 million annual cases of IBD in the United States, 50% of which consists of CD and 50% of UC. Chemokines and cytokines play a pivotal role in the regulation of mucosal inflammation by promoting leukocyte migration to sites of inflammation ultimately leading to tissue damage and destruction. In recent years, experimental studies in rodents have led to a better understanding of the role played by these inflammatory mediators in the development and progression of colitis. However, the clinical literature on IBD remains limited. Therefore, the aim of this study was to evaluate systemic concentrations of key chemokines and cytokines in forty-two IBD patients with a range of disease activity compared to levels found in ten healthy donors. We found a significant increase in an array of chemokines including macrophage migration factor (MIF), CCL25, CCL23, CXCL5, CXCL13, CXCL10, CXCL11, MCP1, and CCL21 in IBD patients as compared to normal healthy donors (P <0.05). Further, we also report increases in the inflammatory cytokines IL-16, IFN-gamma, IL-1 beta and TNF-alpha in IBD patients when compared to healthy donors (P < 0.05). These data clearly indicate an increase in circulating levels of specific chemokines and cytokines that are known to modulate systemic level through immune cells results in affecting local intestinal inflammation and tissue damage in IBD patients. Blockade of these inflammatory mediators should be explored as a mechanism to alleviate or even reverse symptoms of IBD. Published by Elsevier Ltd.
机译：克罗恩氏病（CD）和溃疡性结肠炎（UC）是炎性肠病（IBD）的两种形式，是慢性，复发性和组织破坏性病变，伴有粘膜中效应免疫细胞的失控活化。最新估计表明，美国每年有130万例IBD病例，其中50％由CD构成，而50％由UC构成。趋化因子和细胞因子通过促进白细胞迁移到炎症部位最终导致组织损伤和破坏，在调节粘膜炎症中起关键作用。近年来，在啮齿动物中进行的实验研究已使人们更好地了解了这些炎性介质在结肠炎的发生和发展中所起的作用。然而，关于IBD的临床文献仍然有限。因此，本研究的目的是评估42例IBD患者的关键趋化因子和细胞因子的全身浓度，该疾病的活动范围与十个健康捐献者的水平相比有所不同。我们发现与正常健康捐献者相比，IBD患者中包括巨噬细胞迁移因子（MIF），CCL25，CCL23，CXCL5，CXCL13，CXCL10，CXCL11，MCP1和CCL21在内的一系列趋化因子显着增加（P <0.05）。此外，我们还报告了与健康供体相比，IBD患者的炎性细胞因子IL-16，IFN-γ，IL-1 beta和TNF-α升高（P <0.05）。这些数据清楚地表明，已知通过免疫细胞调节全身水平的特定趋化因子和细胞因子的循环水平增加，导致影响IBD患者的局部肠道炎症和组织损伤。应该探索对这些炎性介质的阻断，以缓解或什至逆转IBD症状。由Elsevier Ltd.发布

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