Expression of intercellular adhesion molecules in the bladder of patients with interstitial cystitis

M Green1, A Filippou, G Sant

  • 1Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Tufts-New England Medical Center, Boston, Massachusetts 02111, USA.

Urology
|April 10, 2004
PubMed

Insights

Interstitial cystitis (IC) bladder biopsies show increased intercellular adhesion molecule-1 (ICAM-1) and other inflammatory markers. These findings correlate with bladder inflammation severity in IC patients.

Area of Science:

  • Urology
  • Immunology
  • Cell Biology

Background:

  • Interstitial cystitis (IC) is a chronic bladder condition causing pain and urinary frequency.
  • Pathological findings in IC bladders include urothelial defects, mast cell activation, and inflammation.
  • Mast cells can trigger inflammation by upregulating cellular adhesion molecules (CAMs).

Purpose of the Study:

  • To investigate the presence of ICAM-1, P-selectin, E-selectin, talin, and vinculin in bladder biopsies from IC patients and controls.
  • To correlate the expression of these molecules with the degree of bladder inflammation in IC.

Main Methods:

  • Immunocytochemical analysis of fresh frozen bladder biopsies.
  • Samples included bladders from female IC patients, normal female bladders, and various control tissues (foreskin, finger skin, transitional cell carcinoma).

Main Results:

  • IC bladder biopsies frequently expressed ICAM-1 (9/10), P-selectin (6/10), vinculin (6/10), talin (5/10), and E-selectin (4/10), primarily perivascularly.
  • Normal bladders showed minimal or no expression of these markers, except faint E-selectin.
  • Control tissues (cancerous bladder/foreskin, inflamed finger) were positive only for ICAM-1.
  • Activated mast cells associated with ICAM-1 were observed in IC samples.

Conclusions:

  • ICAM-1 is significantly expressed in IC bladders.
  • Variable expression of other studied markers suggests a role in the varying inflammatory responses seen in IC.
  • These findings support the involvement of CAMs and inflammation in the pathophysiology of IC.
Abstract