Journal of Translational Medicine (Feb 2022)

Immune cell profiles of patients with interstitial cystitis/bladder pain syndrome

  • Robert M. Moldwin,
  • Vishaan Nursey,
  • Oksana Yaskiv,
  • Siddhartha Dalvi,
  • Eric J. Macdonald,
  • Michael Funaro,
  • Chengliang Zhang,
  • William DeGouveia,
  • Marina Ruzimovsky,
  • Horacio R. Rilo,
  • Edmund J. Miller,
  • Souhel Najjar,
  • Inna Tabansky,
  • Joel N. H. Stern

DOI
https://doi.org/10.1186/s12967-022-03236-7
Journal volume & issue
Vol. 20, no. 1
pp. 1 – 9

Abstract

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Abstract Interstitial cystitis/bladder pain syndrome (IC/BPS) is a disorder characterized by bladder pain upon filling which severely affects quality of life. Clinical presentation can vary. Local inflammatory events typify the clinical presentation of IC/BPS patients with Hunner lesions (IC/BPS-HL). It has previously been proposed that B cells are more prevalent in HL, but understanding their exact role in this environment requires a more complete immunological profile of HL. We characterized immunological dysfunction specifically in HL using immunohistochemistry. We detected significantly more plasma cells (50× increase, p < 0.0001), B cells (28× increase, p < 0.0001), T cells (3× increase, p < 0.0001), monocytes/macrophages (6× increase, p < 0.0001), granulocytes (4× increase, p < 0.0001), and natural killer cells (2× increase, p = 0.0249) in IC/BPS patients with HL than in unaffected controls (UC). Patients with IC/BPS-HL also had significantly elevated urinary levels of IL-6 (p = 0.0054), TNF-α (p = 0.0064) and IL-13 (p = 0.0304) compared to patients with IC/BPS without HL (IC/BPS-NHL). In contrast, IL-12p70 levels were significantly lower in the patients with HL than in those without these lesions (p = 0.0422). Different cytokines were elevated in the urine of IC/BPS patients with and without HL, indicating that different disease processes are active in IC/BPS patients with and without HL. Elevated levels of CD138+, CD20+, and CD3+ cells in HL are consistent B and T-cell involvement in disease processes within HL.