Immune Cell Profiles of Patients with Interstitial Cystitis/Bladder Pain Syndrome - Beyond the Abstract

Interstitial cystitis/Bladder Pain syndrome adversely affects people’s quality of life and function, sometimes to the point of disability. Current epidemiology suggests it to be quite prevalent in the US, with five to 16 million people affected.1 The main symptoms of IC/BPS include pain perceived to be of bladder origin and urinary urgency.1 While some treatments are available, they are often of limited efficacy.2


The pathophysiology and etiology of IC/BPS are unknown, but multiple recent lines of evidence have suggested that the symptoms of some patients may be based upon a local inflammatory process.3,4 Some IC/BPS patients have lesions, termed Hunner lesions (HL), which show an immune cell infiltrate.5,6 Cytokines in the urine of patients with IC/BPS have also been shown to be elevated. Notably, different forms of IC/BPS have different cytokines elevated in the urine, suggesting different immune mechanisms for the disease.7-9

To that end, we have evaluated 48 patients with HL, those patients exhibiting focal inflammatory disease of the bladder wall, to identify the composition of immune cells within the bladder. The largest increase in immune cell percentages within the HL was the presence of plasma cells (50x increase), B cells (28× increase), monocytes/macrophages (6× increase), granulocytes (4× increase), and to a lesser extent T cells (3x increase) and natural killer cells (2× increase) were detected in IC/BPS patients bladder biopsies with HL than in unaffected controls. With this foundational data, scientists can try to identify sub populations of these immune cell types with the bladder of IC/BPS patient to gain insight into the immune cell(s) that may be contributing to the pathophysiology of this disease. Also, the significant increase in B cells, especially plasma cells may indicate a potential antibody component associated with IC/BPS. Eventually, researchers can establish whether IC/BPS is driven by associated antigens that may initiate this disease leading to targeted therapeutic interventions, as there is an arsenal of already-approved treatment available for autoimmune diseases that can be repurposed to help these patients.

Written by: 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

The Smith Institute for Urology, Northwell Health, 450 Lakeville Road New Hyde Park, Lake Success, NY, USA., Department of Neurology, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, USA., Department of Pathology, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, USA., Institute of Molecular Medicine, The Feinstein Institutes for Medical Research, Manhasset, NY, USA., Department of Surgery, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, USA., RDS2 Solutions, Stony Brook, NY, USA., Department of Neurology, Lenox Hill Hospital, New York, NY, USA., The Smith Institute for Urology, Northwell Health, 450 Lakeville Road New Hyde Park, Lake Success, NY, USA.

References:

  1. Duh, K., et al., Crosstalk between the immune system and neural pathways in interstitial cystitis/bladder pain syndrome. Discov Med, 2018. 25(139): p. 243-250.
  2. Hanno, P.M., et al., Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. J Urol, 2015. 193(5): p. 1545-53.
  3. van de Merwe, J.P., Interstitial cystitis and systemic autoimmune diseases. Nat Clin Pract Urol, 2007. 4(9): p. 484-91.
  4. Peeker, R., L. Atanasiu, and Y. Logadottir, Intercurrent autoimmune conditions in classic and non-ulcer interstitial cystitis. Scand J Urol Nephrol, 2003. 37(1): p. 60-3.
  5. Gamper, M., et al., Local immune response in bladder pain syndrome/interstitial cystitis ESSIC type 3C. Int Urogynecol J, 2013. 24(12): p. 2049-57. PMCID: PMC3838592
  6. Maeda, D., et al., Hunner-Type (Classic) Interstitial Cystitis: A Distinct Inflammatory Disorder Characterized by Pancystitis, with Frequent Expansion of Clonal B-Cells and Epithelial Denudation. PLoS One, 2015. 10(11): p. e0143316. PMCID: PMC4654580
  7. Lotz, M., et al., Interleukin-6 and interstitial cystitis. J Urol, 1994. 152(3): p. 869-73.
  8. Saban, R., et al., Urothelial expression of neuropilins and VEGF receptors in control and interstitial cystitis patients. Am J Physiol Renal Physiol, 2008. 295(6): p. F1613-23. PMCID: PMC2604836
  9. Moldwin, R.M., et al., Immune Cell Profiles and Cytokine Levels of Patients with Interstitial Cystitis/Bladder Pain Syndrome, J Transl Med, 2022. 20, 97.

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