Chemokine and cytokine levels in inflammatory bowel disease patients.

Chemokine and cytokine levels in inflammatory bowel disease patients.
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DOI:
10.1016/j.cyto.2015.10.008
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发表时间:
2016-01
期刊:
影响因子:
3.8
通讯作者:
Nagarkatti PS
Nagarkatti PS
中科院分区:
医学3区
文献类型:
--
作者:
Singh UP;Singh NP;Murphy EA;Price RL;Fayad R;Nagarkatti M;Nagarkatti PS

文献摘要

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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、复发性和组织破坏性病变,其伴随着粘膜中效应免疫细胞的不受控制的活化。最近的估计表明,美国每年有130万例IBD病例,其中50%由CD组成,50%由UC组成。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而在调节粘膜炎症中起关键作用。近年来,在啮齿动物中的实验研究使人们更好地理解了这些炎症介质在结肠炎发展和进展中所起的作用。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例具有一系列疾病活动性的IBD患者的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患者中一系列趋化因子包括巨噬细胞迁移因子(MIF)、CCL 25、CCL 23、CXCL 5、CXCL 13、CXCL 10、CXCL 11、MCP 1和CCL 21显著增加(P < 0.05)。此外,我们还报告了IBD患者中炎性细胞因子IL-16、IFN-γ、IL-1β和TNF-α与健康供体相比增加(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的增加导致影响IBD患者中的局部肠道炎症和组织损伤。这些炎症介质的阻断应该被探索作为缓解甚至逆转IBD症状的机制。
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.