The Lipid-Inflammation Link in Benign Prostatic Hyperplasia - a Correlation Analysis of Concurrent Pathologies in Enucleated Prostate Tissues
Poster #: 188
Session/Time: A
Author:
Dita Julianingsih, BS, MS
Mentor:
Petra Popovics, MS, PhD
Research Type: Basic Science
Abstract
INTRODUCTION:
Benign prostatic hyperplasia (BPH) is characterized by pathological changes including fibrosis, inflammation, smooth muscle dysfunction, and epithelial proliferation. Our previous studies identified lipid accumulation as a novel pathological feature of BPH, but its relationship to other pathologies, such as inflammation and fibrosis, remains poorly understood. Therefore, this study aimed to investigate how lipid deposition relates to pathological and clinical characteristics of BPH.
METHODS:
Prostate tissues from 44 BPH patients undergoing Holmium Laser Enucleation of the Prostate surgery were analyzed. Lipids were visualized with Oil Red O staining, immune cell infiltration quantified by CD45⁺ (total immune cells) and CD68⁺ (macrophages) immunohistochemistry, and collagen accumulation (fibrosis marker) assessed by Picrosirius Red staining. Glandular percentage was analyzed from H&E staining. Images were analyzed using Inform software, and associations between variables were evaluated by Spearman correlation.
RESULTS:
Lipid accumulation exhibited a strong positive relationship with PSA levels (r = 0.78, p < 0.0001) and glandular proportion (r = 0.60, p < 0.0001), and also showed a significant positive correlation with prostate size (r = 0.51, p = 0.0007), CD45⁺ immune cell infiltration (r = 0.50, p = 0.0009), and CD68⁺ macrophage presence (r = 0.33, p = 0.037). In contrast, collagen intensity was inversely correlated with lipid accumulation (r = -0.52, p = 0.00046).
CONCLUSION:
These findings provide the first evidence that prostatic lipid accumulation is associated with both prostatic inflammation and prostate growth. In contrast, fibrosis appears to be primarily linked to a smaller prostatic BPH phenotype and is inversely correlated with prostatic lipid content. Our future studies will investigate the mechanistic connections between lipid metabolism and immune activation and assess whether targeting lipid pathways may provide new therapeutic strategies for BPH.
Benign prostatic hyperplasia (BPH) is characterized by pathological changes including fibrosis, inflammation, smooth muscle dysfunction, and epithelial proliferation. Our previous studies identified lipid accumulation as a novel pathological feature of BPH, but its relationship to other pathologies, such as inflammation and fibrosis, remains poorly understood. Therefore, this study aimed to investigate how lipid deposition relates to pathological and clinical characteristics of BPH.
METHODS:
Prostate tissues from 44 BPH patients undergoing Holmium Laser Enucleation of the Prostate surgery were analyzed. Lipids were visualized with Oil Red O staining, immune cell infiltration quantified by CD45⁺ (total immune cells) and CD68⁺ (macrophages) immunohistochemistry, and collagen accumulation (fibrosis marker) assessed by Picrosirius Red staining. Glandular percentage was analyzed from H&E staining. Images were analyzed using Inform software, and associations between variables were evaluated by Spearman correlation.
RESULTS:
Lipid accumulation exhibited a strong positive relationship with PSA levels (r = 0.78, p < 0.0001) and glandular proportion (r = 0.60, p < 0.0001), and also showed a significant positive correlation with prostate size (r = 0.51, p = 0.0007), CD45⁺ immune cell infiltration (r = 0.50, p = 0.0009), and CD68⁺ macrophage presence (r = 0.33, p = 0.037). In contrast, collagen intensity was inversely correlated with lipid accumulation (r = -0.52, p = 0.00046).
CONCLUSION:
These findings provide the first evidence that prostatic lipid accumulation is associated with both prostatic inflammation and prostate growth. In contrast, fibrosis appears to be primarily linked to a smaller prostatic BPH phenotype and is inversely correlated with prostatic lipid content. Our future studies will investigate the mechanistic connections between lipid metabolism and immune activation and assess whether targeting lipid pathways may provide new therapeutic strategies for BPH.