Serum Zonulin and Its Role in Rosacea Pathogenesis: A Comprehensive Estimation Study

血清中肠促胰岛素及其在酒渣鼻发病机制中的作用:一项综合评估研究

阅读:2

Abstract

INTRODUCTION: Rosacea is a chronic inflammatory skin disorder distinguished by recurrent episodes of inflammatory papules, persistent erythema, facial flushing, pustules, and telangiectasia. Any disturbance in the gut microbiome could influence the immune system equilibrium in rosacea by releasing zonulin, leading to increased intestinal permeability and the passage of many microbes into the circulation, causing inflammation. OBJECTIVES: We aimed to estimate the serum zonulin levels in cases with rosacea compared with healthy controls. Some fecal bacteria were investigated in an attempt to find a relationship between gut microbiome and rosacea. METHODS: This case-control study was performed on 42 participants aged above 18 years: 21 patients with a clinical diagnosis of rosacea approved by dermoscopy and 21 healthy individuals as controls. The serum zonulin level was estimated by the enzyme-linked immunosorbent assay technique, and some gut microbiomes were investigated using real-time quantitative PCR. RESULTS: There was a statistically significantly higher serum zonulin level in rosacea cases than in controls. There was a statistically significant elevation in Bacteroides and Lactobacillus gut microbiomes in rosacea patients compared to controls, while there was no statistically significant increase in Fusobacterium microbiome in patients. Zonulin levels did not show a significant correlation with gut microbiome. CONCLUSIONS: Serum zonulin measurement can be used as a discriminating marker between rosacea and healthy controls, due to getting a specific cut-off point in ROC analysis with the highest specificity and sensitivity (100% and 100%, respectively). Gut microbial dysbiosis could play a valuable role in the disease pathogenesis.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。