Epithelial Barrier Breakdown and Its Link to Luminal Macrophage Translocation in BPH
Poster #: 183
Session/Time: B
Author:
Leah R. Butler, BS
Mentor:
Petra Popovics, MS, PhD
Research Type: Basic Science
Abstract
INTRODUCTION:
Benign prostatic hyperplasia is a prevalent urologic condition in aging men that contributes to lower urinary tract symptoms. While its underlying mechanisms remain unclear, epithelial barrier dysfunction has emerged as a potential contributor. E-cadherin, a key cell-cell adhesion protein, plays a central role in maintaining epithelial morphology and barrier integrity. We hypothesized that downregulation of E-cadherin in BPH tissues contributes to epithelial weakening and increased permeability.
METHODS:
A total of 43 patients who underwent Holmium Laser Enucleation of the Prostate were included in this study. Prostate tissues were formalin-fixed and paraffin-embedded.Immunohistochemistry staining was performed using rabbit anti-E-cadherin as primary antibody (clone EP700Y, 1:10,000 dilution) following blocking with horse serum. A horse anti-rabbit secondary antibody was applied, and detection was carried out using HRP/DAB detection. Imaging was conducted using the Mantra Pathological Imaging System. Quantitative analysis of epithelial segmentation and E-cadherin staining intensity was performed using InForm and Prism software. Clinical variables included patient age, BMI, prostate-specific antigen levels, treatment type and histological tissue characteristics.
RESULTS:
Simple linear regression analysis showed no statistically significant correlation between E-cadherin staining intensity and patient age, BMI, or treatment type. When patients were grouped by treatment alpha-blockers, 5-alpha-reductase inhibitors, combination therapy, and other therapies no significant variation in E-cadherin intensity was observed. Additionally, E-cadherin staining intensity did not correlate with immune cell infiltration or prostate pathology markers, including CD68+, CD45+, and PSR. These findings suggest that E-cadherin intensity alone is not sufficient to differentiate clinical or treatment-related patterns in BPH pathology.
CONCLUSION:
While epithelial barrier weakening remains a promising hypothesis in BPH progression, our results indicate that E-cadherin intensity may not correlate strongly with clinical variables or treatment history. Future work will focus on evaluating tight junction markers such as ZO-1 and β-catenin redistribution, as well as the spatial co-localization of CD68+ macrophages with epithelial defects, to further explore barrier disruption and immune infiltration mechanisms in BPH.
Benign prostatic hyperplasia is a prevalent urologic condition in aging men that contributes to lower urinary tract symptoms. While its underlying mechanisms remain unclear, epithelial barrier dysfunction has emerged as a potential contributor. E-cadherin, a key cell-cell adhesion protein, plays a central role in maintaining epithelial morphology and barrier integrity. We hypothesized that downregulation of E-cadherin in BPH tissues contributes to epithelial weakening and increased permeability.
METHODS:
A total of 43 patients who underwent Holmium Laser Enucleation of the Prostate were included in this study. Prostate tissues were formalin-fixed and paraffin-embedded.Immunohistochemistry staining was performed using rabbit anti-E-cadherin as primary antibody (clone EP700Y, 1:10,000 dilution) following blocking with horse serum. A horse anti-rabbit secondary antibody was applied, and detection was carried out using HRP/DAB detection. Imaging was conducted using the Mantra Pathological Imaging System. Quantitative analysis of epithelial segmentation and E-cadherin staining intensity was performed using InForm and Prism software. Clinical variables included patient age, BMI, prostate-specific antigen levels, treatment type and histological tissue characteristics.
RESULTS:
Simple linear regression analysis showed no statistically significant correlation between E-cadherin staining intensity and patient age, BMI, or treatment type. When patients were grouped by treatment alpha-blockers, 5-alpha-reductase inhibitors, combination therapy, and other therapies no significant variation in E-cadherin intensity was observed. Additionally, E-cadherin staining intensity did not correlate with immune cell infiltration or prostate pathology markers, including CD68+, CD45+, and PSR. These findings suggest that E-cadherin intensity alone is not sufficient to differentiate clinical or treatment-related patterns in BPH pathology.
CONCLUSION:
While epithelial barrier weakening remains a promising hypothesis in BPH progression, our results indicate that E-cadherin intensity may not correlate strongly with clinical variables or treatment history. Future work will focus on evaluating tight junction markers such as ZO-1 and β-catenin redistribution, as well as the spatial co-localization of CD68+ macrophages with epithelial defects, to further explore barrier disruption and immune infiltration mechanisms in BPH.