Immunological Interactions and Inflammatory Changes in the Pathways of Benign Prostatic Hyperplasia and Prostate Cancer
The prostate is unity of the accessory glands in the male reproductive system and plays a crucial role in maintaining sperm vitality by secreting components that form part of the semen. Prostate diseases, such as benign prostatic hyperplasia (BPH) and prostate cancer (PCa), are associated with inflammatory changes that affect male fertility. Research suggests that prostatitis may be a precursor to the development of these conditions. The study included 84 men aged 35-79 years, divided into three groups: benign prostatic hyperplasia (HP), prostate cancer (PCa), and a control group. Cytokine concentrations of IL-6, IL-8, TNF-α, and C-reactive protein were measured using ELISA. The results showed significant differences between groups in IL-8 levels, with the prostate cancer group recording the highest concentration. No significant differences were observed in IL-6 levels. Significant differences were noted in TNF-α and C-reactive protein levels between groups. Previous research highlights the role of cytokines in the development of prostate cancer, but data on their specific role is limited. Elevated IL-6 and IL-8 levels are associated with increased prostate-specific antigen (PSA) and disease progression. Moreover, elevated TNF-α and C-reactive protein levels are linked to in assistance of benign and malignant prostatic hyperplasia. This study provides additional evidence of the role of cytokines in the development of prostate diseases, underscoring the importance of targeting these molecules in diagnosis and treatment.
Authors
- Saif Ali (ORCID: https://orcid.org/0000-0002-6720-6164)
- Omar Raheem Khalaf AL-Obaidi
- Mostafa Ali Abdulrahman
Institutions
- University of Samarra (IQ)
Publication Details
- Journal
- Samarra Journal of Pure and Applied Science
- Published
- 2025-06-30
- DOI
- https://doi.org/10.54153/sjpas.2025.v7i2.1026
- Primary Topic
- Prostate Cancer Treatment and Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00