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Mast cell function in prostate inflammation, fibrosis, and smooth muscle cell dysfunction.

Goutham Pattabiraman1, Ashlee J Bell-Cohn1, Stephen F Murphy1

  • 1Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

American Journal of Physiology. Renal Physiology
|August 23, 2021
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Summary

Mast cells drive prostate inflammation and urinary dysfunction in a mouse model of benign prostatic hyperplasia (BPH). Inhibiting mast cells reduced symptoms and reversed prostate pathology, suggesting a new therapeutic target for BPH and lower urinary tract symptoms (LUTS).

Keywords:
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Area of Science:

  • Urology
  • Immunology
  • Pathophysiology

Background:

  • Benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) involve prostate inflammation, fibrosis, and smooth muscle contraction.
  • Mast cells are implicated in LUTS pathophysiology, but their precise role requires further elucidation.
  • Uropathogenic *Escherichia coli* (CP1) infection in mice models key aspects of BPH/LUTS.

Purpose of the Study:

  • To investigate the role of mast cells in the pathophysiology of CP1-induced prostate inflammation and urinary dysfunction.
  • To evaluate the therapeutic potential of mast cell inhibition for BPH/LUTS.

Main Methods:

  • Intraurethral inoculation of mice with uropathogenic *Escherichia coli* (CP1).
  • Therapeutic intervention using a combination of cromolyn sodium (mast cell stabilizer) and cetirizine di-hydrochloride (histamine 1 receptor antagonist).
  • Assessment of prostate pathology, immune cell infiltration, fibrosis, inflammation, and urinary function.
  • Measurement of myosin light chain-2 phosphorylation as a marker of smooth muscle contraction.

Main Results:

  • CP1 infection induced prostate inflammation, fibrosis, mast cell activation, and urinary dysfunction in mice.
  • Mast cell inhibition significantly alleviated urinary dysfunction and reduced prostate inflammation, fibrosis, and immune cell infiltration.
  • Treated mice exhibited reduced myosin light chain-2 phosphorylation, indicating decreased smooth muscle contraction.

Conclusions:

  • Mast cells play a critical role in the pathophysiology of urinary dysfunction associated with BPH/LUTS.
  • Therapeutic inhibition of mast cells effectively alleviates prostate pathology and urinary symptoms in a mouse model.
  • Mast cell inhibition represents a promising therapeutic strategy for preventing and reversing BPH/LUTS pathology and symptoms.