Complement activation by autoantigen recognition in the growth process of benign prostatic hyperplasia

Area of Science:

• Urology
• Immunology
• Pathophysiology

Background:

• The underlying mechanisms of benign prostatic hyperplasia (BPH) pathophysiology are not fully understood.
• Complement system activation is implicated in various inflammatory conditions.

Purpose of the Study:

• To investigate the role of complement activation in benign prostatic hyperplasia (BPH) development.
• To explore the involvement of autoantibodies in BPH pathogenesis using a rat model.

Main Methods:

• Analysis of complement components (C1q, C3, MBL, FB, C5b-9) and IgG deposition in rat and human BPH tissues using RT-PCR, Western blotting, and immunohistochemistry (IHC).
• ELISA for serum IgG levels and immunoprecipitation to identify IgG autoantibody targets in the rat model.

Main Results:

• Rat BPH tissues showed high localization of C1q, C3, MBL, FB, and C5b-9.
• Human BPH tissues exhibited abundant C3, FB, and C5b-9, but not C1q or MBL.
• IgG autoantibodies targeting heat shock protein 90, annexin, α-smooth muscle actin, and β-actin were identified in the rat BPH model.

Conclusions:

• Complement activation is strongly suggested to be involved in the growth process of BPH.
• Classical pathway activation, potentially triggered by autoantibodies, may drive BPH progression.