在炎症性肠道疾病中,CCL20表达升高,并且由维生素D代谢产物减弱
Johannes Stallhofer1, Felix Reichl2, Michael Lauseker3
1Department of Internal Medicine IV, Jena University Hospital, Am Klinikum 1, 07747, Jena, Germany. johannes.stallhofer@med.uni-jena.de.
在炎症性肠病 (IBD) 患者中,维生素D缺乏会提高CCL20水平. 虽然维生素D可以调节健康个体和性结肠炎的CCL20,但这种效果在克罗恩病患者中受损.
科学领域:
- 胃肠道学和免疫学
- 营养科学 营养科学
- 分子生物学分子生物学
背景情况:
- CCL20是一种Th17细胞化学吸引剂,在炎症性肠病 (IBD) 中过度表达,并且与克罗恩病中的NOD2突变有关.
- 维生素D代谢产物因其减轻IBD症状的潜力而得到认可.
- 维生素D状态,CCL20表达和IBD之间的相互作用,特别是NOD2突变的克罗恩病,需要进一步研究.
研究的目的:
- 调查维生素D缺乏是否会增加IBD患者和健康对照者的循环CCL20水平.
- 为了确定活性1,25-二氧维生素D () 是否降低系统和肠道CCL20表达的调节.
- 探索NOD2突变和维生素D状态对克罗恩病中CCL20水平的影响.
主要方法:
- 在170名克罗恩氏病患者,80名性结肠炎患者和60名健康对照人群中测量血清CCL20,25-氧维生素D和酸的截面研究.
- 在克罗恩病患者中对NOD2突变的基因定型.
- 在体外实验中评估酸对人类肠道上皮细胞HT-29细胞中CCL20表达的影响.
主要成果:
- 无论是IBD诊断还是维生素D缺乏,都与CCL20水平升高独立相关.
- 克罗恩病和性结肠炎患者的CCL20显著高于健康对照组.
- 酸抑制了肠表皮CCL20的诱导;胆酸补充剂降低了克罗恩氏病患者的CCL20,而不考虑NOD2突变.
结论:
- 维生素D缺乏导致IBD中CCL20升高.
- 在健康对照组和性结肠炎患者中,醇显示出降低CCL20的潜力.
- 维生素D代谢物对CCL20的调节作用在克罗恩病患者中似乎受损,这表明它是一个潜在的治疗点.
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