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炎症性肠病患者体内趋化因子和细胞因子水平

Chemokine and cytokine levels in inflammatory bowel disease patients.

作者信息

Singh Udai P, Singh Narendra P, Murphy E Angela, Price Robert L, Fayad Raja, Nagarkatti Mitzi, Nagarkatti Prakash S

机构信息

Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.

Department of Pathology, Microbiology and Immunology, School of Medicine, University of South Carolina, Columbia, SC 29208, USA.

出版信息

Cytokine. 2016 Jan;77:44-9. doi: 10.1016/j.cyto.2015.10.008. Epub 2015 Oct 29.

Abstract

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-γ, IL-1β and TNF-α 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.

摘要

克罗恩病(CD)和溃疡性结肠炎(UC)是炎症性肠病(IBD)的两种形式,是慢性、复发性且具有组织破坏性的病变,伴有黏膜中效应免疫细胞的失控激活。最近的估计表明,美国每年有130万例IBD病例,其中50%为CD,50%为UC。趋化因子和细胞因子通过促进白细胞迁移至炎症部位,最终导致组织损伤和破坏,在黏膜炎症调节中起关键作用。近年来,对啮齿动物的实验研究使人们对这些炎症介质在结肠炎发生和发展中所起的作用有了更好的理解。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例具有一系列疾病活动度的IBD患者体内关键趋化因子和细胞因子的全身浓度,并与10名健康供体的水平进行比较。我们发现,与正常健康供体相比,IBD患者体内一系列趋化因子显著增加,包括巨噬细胞迁移因子(MIF)、CCL25、CCL23、CXCL5、CXCL13、CXCL10、CXCL11、MCP1和CCL21(P<0.05)。此外,与健康供体相比,我们还发现IBD患者体内炎症细胞因子IL-16、IFN-γ、IL-1β和TNF-α也有所增加(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升高,会导致IBD患者局部肠道炎症和组织损伤。应探索阻断这些炎症介质作为缓解甚至逆转IBD症状的一种机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6cb/4666758/4b7718a51d94/nihms734638f1.jpg

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