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Abstract
Exploring the causal relationship between gut microbiota and benign prostatic hyperplasia: 16S rRNA and Mendelian randomization analysis
Non-Moderated Poster Abstract
Clinical Research
Benign Prostate Hyperplasia and Male Lower Urinary Tract Symptoms: Medical Treatment
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China
Bohan Lin 1278053784@qq.com The First Affiliated Hospital of Fujian Medical University Urology Fuzhou China *
Ning Xu drxun@fjmu.edu.cn The First Affiliated Hospital of Fujian Medical University Urology Fuzhou China -
Yong Wei weiyong2017@fjmu.edu.cn The First Affiliated Hospital of Fujian Medical University Urology Fuzhou China -
Xue-Yi Xue xuexueyi@fjmu.edu.cn The First Affiliated Hospital of Fujian Medical University Urology Fuzhou China -
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Abstract Content
Recent studies have highlighted a potential correlation between the gut microbiota (GM) and benign prostatic hyperplasia (BPH), while the causal relationship remains uncertain. This study aims to explore the potential causal relationship between GM and BPH.
A two-sample mendelian randomization (MR) analysis was conducted utilizing data from the most extensive GM-focused genome-wide association studies (GWASs) by the MiBioGen consortium, with a sample size of 18,340. The summary-level GWAS data for BPH, encompassing 13118 cases and 72799 controls, were sourced from the FinnGen consortium. The inverse variance-weighted (IVW) method was employed as the primary approach to evaluate the causal relationship between GM and BPH, with supplementary methods including MR-Egger and weighted median (WM). To evaluate the robustness of the findings and the strength of the causal associations, sensitivity analyses were performed, including tests for heterogeneity, horizontal pleiotropy, and leave-one-out sensitivity analysis. Fecal samples were collected from BPH patients and healthy male controls for 16S rRNA sequencing to validate the findings of MR analysis.
Bidirectional MR results confirmed a causal relationship between specific GM and BPH. 16S rRNA sequencing revealed significant differences in gut microbiota composition between cases and controls. The IVW results revealed that Fecalibacterium [odds ratio (OR)=1.482, 95%CI: 1.161-1.893, P=0.002], Bacteroides (OR=1.749, 95%CI: 1.261-2.426, P=0.001), and Prevotella (OR=1.394, 95%CI: 1.097-1.771, P=0.007) were positively associated with BPH risk; whereas Ruminococcus gnavus (OR: 0.882, 95% CI: 0.784-0.992, P=0.037), Firmicutes (OR: 0.742, 95% CI: 0.617-0.892, P=0.002), and Aminoacidobacteria (OR: 0.751, 95% CI: 0.594-0.948, P=0.016) exhibited negative correlations with BPH risk. Reverse MR analysis indicated that the six GM were not significantly influenced by BPH, and no significant heterogeneity or horizontal pleiotropy was observed among the instrumental variables.
Our MR study highlights a potential causal relationship between GM and BPH. These findings may provide new insights into the pathogenesis of BPH and offer valuable perspectives for the development of novel preventative and therapeutic strategies.
benign prostatic hyperplasia; gut microbiota; Mendelian randomization; causal relationship; genome-wide association study
 
 
 
 
 
 
 
 
 
 
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