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肠易激综合征腹泻型患者中 dectin-1 与肥大细胞的关系。

The relationship between dectin-1 and mast cells in patients with diarrhea-predominant irritable bowel syndrome.

机构信息

Department of Gastroenterology, Peking University First Hospital, Beijing, China.

出版信息

Scand J Gastroenterol. 2020 Jul;55(7):762-768. doi: 10.1080/00365521.2020.1774925. Epub 2020 Jun 4.

Abstract

Currently, the role of the microbiome GBA is being widely studied in the pathogenesis of visceral hypersensitivity in IBS. To investigate the role of fungus, the current study aimed to i) investigate the expression of Syk/CARD9-coupled Dectin-1 receptors in the ileocecal mucosa in D-IBS patients and (ii) explore the relationships between Dectin-1 and plasma MCT levels as well as anorectal sensory function in patients with D-IBS. Thirty-eight D-IBS patients who met the Rome III criteria and 2 groups of age- and sex-matched asymptomatic healthy controls were recruited from March 2015 to January 2017. Anorectal sensory function was quantified by HR-ARM. Plasma MCT titers were identified by ELISA, while the expression of Syk/CARD9 Dectin-1 receptors in ileocecal mucosa was identified by RT-qPCR. (i) The expression of Syk/CARD9-coupled Dectin-1 receptors was significantly higher in D-IBS patients than in controls ( < .001). ii) The threshold values of first sensation and desire to defecate were significantly lower in D-IBS patientsthan in controls (the P value was0.007 and 0.001 respectively). (iii) There were negative correlations between plasma MCT levels and first sensation thresholds in D-IBS patients ( = -0.513,  = .012) and the desire to defecate thresholds ( = -0.423,  = .044). (iiii) There was a positive correlation between plasma MCT titers and the expression of Dectin-1 receptors in D-IBS patients ( = 0.565,  = .005). These results suggested that fungi may partially participate in the genesis of visceral hypersensitivity by activating mast cells, which is mediated by activation of the Dectin-1 receptor-mediated Syk/CARD9 signaling pathway.

摘要

目前,微生物组 GBA 在 IBS 内脏高敏性的发病机制中的作用正在被广泛研究。为了研究真菌的作用,本研究旨在:i)研究 D-IBS 患者回盲部黏膜中 Syk/CARD9 偶联的 Dectin-1 受体的表达;ii)探讨 Dectin-1 与血浆 MCT 水平以及 D-IBS 患者肛门直肠感觉功能的关系。从 2015 年 3 月至 2017 年 1 月,招募了 38 名符合罗马 III 标准的 D-IBS 患者和 2 组年龄和性别匹配的无症状健康对照者。通过 HR-ARM 量化肛门直肠感觉功能。通过 ELISA 鉴定血浆 MCT 滴度,通过 RT-qPCR 鉴定回肠黏膜中 Syk/CARD9 Dectin-1 受体的表达。i)D-IBS 患者的 Syk/CARD9 偶联 Dectin-1 受体的表达明显高于对照组(<0.001)。ii)D-IBS 患者的首次感觉和排便欲望阈值明显低于对照组(P 值分别为 0.007 和 0.001)。iii)D-IBS 患者的血浆 MCT 水平与首次感觉阈值之间存在负相关(= -0.513,=0.012)和排便欲望阈值(= -0.423,=0.044)。iv)D-IBS 患者的血浆 MCT 滴度与 Dectin-1 受体的表达呈正相关(=0.565,=0.005)。这些结果表明,真菌可能通过激活肥大细胞部分参与内脏高敏性的发生,这是由 Dectin-1 受体介导的 Syk/CARD9 信号通路的激活介导的。

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