4.3 Article

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

期刊

SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
卷 55, 期 7, 页码 762-768

出版社

TAYLOR & FRANCIS LTD
DOI: 10.1080/00365521.2020.1774925

关键词

Dectin-1 receptors; fungus; mast cells; visceral hypersensitivity; IBS

资金

  1. Natural Science Foundation of Beijing Municipality [7152147]

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Background/Aims: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. Methods: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. Results:(i) The expression of Syk/CARD9-coupled Dectin-1 receptors was significantly higher in D-IBS patients than in controls (p < .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 (r= -0.513,p = .012) and the desire to defecate thresholds (r= -0.423,p = .044). (iiii) There was a positive correlation between plasma MCT titers and the expression of Dectin-1 receptors in D-IBS patients (r = 0.565,p = .005). Conclusions: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.

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