The immune system in Interstitial Cystitis/Bladder Pain Syndrome and therapeutic agents

Abstract

Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) is defined by bladder pain and lower urinary tract symptoms (LUTS) in the absence of a definable etiology. Urinary tract infection is not the only definable etiology. Multiple clinical phenotypes appear within the IC/BPS patient population (Clemens, 2019) . This is likely the reason that an etiology for the disorder has not yet been identified. The heterogeneity of this population is also the probable cause for multiple failures of therapeutic trials (Nickel and Moldwin, 2018). One IC/BPS phenotype that is readily distinguishable on cystoscopy is characterized by Hunner lesions: focal, erythematous mucosal patches with abnormal capillary architecture, edema, and scattered hemorrhages. (Akiyama et al., 2019) Current evidence suggests both local and/or centralized pathologic processes may be associated with pain experienced in IC/BPS (IC/BPS), the formation of bladder lesions is an identifiable local event in patients with IC/BPS with Hunner lesion (IC/BPS-HL). (Lai, 2021) This review will highlight recent developments in understanding the pathophysiology of IC/BPS as it relates to the immune system. We will discuss relevant immune cells, gene expression profiles, cytokine milieu, and relevant treatment modalities.

Keywords

• Interstitial Cystitis
• Hunner lesion
• Bladder Pain Syndrome
• Immune system
• Biomarkers
• IC/BPS treatment