The association between overactive bladder and systemic immunity-inflammation index: a cross-sectional study of NHANES 2005 to 2018.

Current research indicate that inflammation is linked to the development of overactive bladder (OAB). The aim of this study was to examine the correlation between OAB and the systemic immunity-inflammation index (SII) in the USA. We analyzed data from 31,881 participants in the National Health and Nutrition Examination Survey 2005-2018. SII, calculated as platelet count × neutrophil count/lymphocyte count, was categorized into quartiles. OAB was defined by the presence of urge urinary incontinence and nocturia. Weighted logistic regression models were used to examine the independent relationship between SII and OAB, adjusting for demographic factors, kidney function, and diabetes status. The results showed that each tenfold increase in log-transformed SII was associated with an 18% higher odds of OAB (OR 1.18, 95% CI 1.08-1.28) in the fully adjusted model. Compared to the lowest SII quartile, the highest quartile had a 28% increased OAB risk (OR 1.28, 95% CI 1.12-1.47). The positive association between SII and OAB risk was consistently observed across subgroups stratified by age, sex, race, marital status, education, and poverty level. Our study reveals a positive correlation between SII levels and OAB, indicating that higher SII levels are associated with an increased likelihood of developing OAB.

The Pharmacological Mechanism of Diabetes Mellitus-Associated Overactive Bladder and Its Treatment with Botulinum Toxin A.

Diabetes mellitus (DM) is an independent risk factor for overactive bladder (OAB). The pathophysiology of DM-associated OAB is multifactorial and time-dependent. Diabetic bladder dysfunction is highly associated with diabetic complications, mainly including diabetic neuropathy and atherosclerosis. Chronic systemic inflammation and bladder urothelial inflammation may contribute to the onset of OAB. Intravesical botulinum toxin A (BoNT-A) injection has proved to be a successful treatment for idiopathic and neurogenic OAB. BoNT-A can inhibit the efferent pathways of the bladder as well as the chronic inflammation and hypersensitivity via the afferent pathways. We conducted a review of the published literature in Pubmed using a combination of two keywords, namely "botulinum toxin A" (BoNT-A) and "overactive bladder", with or without the additional keywords "detrusor overactivity", "diabetes mellitus", "inflammation", and "urodynamic study". We also reviewed the experience of our research teams, who have published several studies of the association between DM and OAB. Since limited data support the effectiveness and safety of BoNT-A for treating patients with DM-associated OAB, a comprehensive evaluation of diabetic complications and urodynamic study is needed before treatment. In the future, it is imperative to explore the clinical characteristics and inflammatory biomarkers of diabetes as determining predictors of the treatment efficacy.

Local immune response in bladder pain syndrome/interstitial cystitis ESSIC type 3C.

INTRODUCTION AND HYPOTHESIS: Bladder pain syndrome/interstitial cystitis (BPS/IC) is identified based on subjective symptoms which lead to heterogeneous patient populations. Previous studies using gene expression arrays for BPS/IC with Hunner's lesions [European Society for the Study of Interstitial Cystitis (ESSIC) type 3C], a subtype of the condition discernible by cystoscopy, have revealed characteristic immune responses and urothelial abnormalities. This current study aimed to further characterize this subtype using a gene expression panel. We hypothesized that B-cell activation with high levels of urinary antibody concentration would be found. METHODS: Cold-cup bladder biopsies, catheterized urine and blood were collected from 15 BPS/IC ESSIC type 3C patients, 11 non-inflammatory overactive bladder (OAB) patients and eight healthy controls. Gene expression in biopsies was quantified by real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemistry was performed on bladder tissue and urinary immunoglobulins G and A were quantified by enzyme-linked immunosorbent assay. Statistical analyses included the Kruskal-Wallis test for non-parametric data and post hoc tests identified differences between groups. RESULTS: High expression of T- and B-cell markers (CTLA4, CD20, CD79A, IGH@), low expression of urothelial markers (KRT20, UPK1B, UPK3A), focal lymphoid aggregates in the submucosa and high immunoglobulin concentration in urine were found exclusively in BPS/IC ESSIC type 3C patients. Results for OAB were in intermediate ranges between the other two groups and UPK1B even reached significantly lower expression when compared to healthy controls. CONCLUSIONS: BPS/IC ESSIC type 3C is characterized by a local adaptive immune response with elevated urinary antibody concentrations. Quantification of urinary immunoglobulin levels could be used for a non-invasive diagnosis of BPS/IC ESSIC type 3C.

Immunological and viral features in patients with overactive bladder associated with human T-cell lymphotropic virus type 1 infection.

The majority of patients infected with human T-cell lymphotropic virus-type 1 (HTLV-1) are considered carriers, but a high frequency of urinary symptoms of overactive bladder, common in HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) have been documented in these patients. The aim of this study was to determine if immunological and viral factors that are seen in HAM/TSP are also observed in these patients. Participants were classified as HTLV-1 carriers (n = 45), HTLV-1 patients suffering from overactive bladder (n = 45) and HAM/TSP (n = 45). Cells from HTLV-1 overactive bladder patients produced spontaneously more proinflammatory cytokines than carriers. TNF-α and IL-17 levels were similar in HAM/TSP and HTLV-1 overactive bladder patients. High proviral load was found in patients with overactive bladder and HAM/TSP and correlated with proinflammatory cytokines. In contrast with findings in patients with HAM/TSP, serum levels of Th1 chemokines were similar in HTLV-1 overactive bladder and carriers. Exogenous addition of regulatory cytokines decreased spontaneous IFN-γ production in cell cultures from HTLV-1 overactive bladder patients. The results show that HTLV-1 overactive bladder and HAM/TSP patients have in common some immunological features as well as similar proviral load profile. The data show that HTLV-1 overactive bladder patients are still able to down regulate their inflammatory immune response. In addition, these patients express levels of chemokines similar to carriers, which may explain why they have yet to develop the same degree of spinal cord damage as seen in patients with HAM/TSP. These patients present symptoms of overactive bladder, which may be an early sign of HAM/TSP.

Differences in mast cell infiltration, E-cadherin, and zonula occludens-1 expression between patients with overactive bladder and interstitial cystitis/bladder pain syndrome.

OBJECTIVE: To investigate the difference of infiltration of mast cells and the distribution of protein involved in the urothelial barrier function between patients with overactive bladder syndrome (OAB) and interstitial cystitis/bladder pain syndrome (IC/BPS). METHODS: Bladder wall biopsies were performed in 27 patients with OAB, 18 patients with IC/BPS, and 19 controls. The expression of junction protein E-cadherin, tight junction protein zonula occludens (ZO-1), and activated mast cells in the bladder wall were evaluated quantitatively using immunofluorescence staining. RESULTS: The numbers of mast cells in the urothelium and suburothelium areas were low in the control group (mean ± standard error 1.77 ± 0.47). A highly significant increase in mast cell infiltration was observed in OAB (4.00 ± 0.55, P = .002) and IC/BPS specimens (4.64 ± 0.72, P = .000). ZO-1 expression was significantly decreased in IC/PBS (7.45 ± 0.99) compared with OAB (13.46 ± 1.32, P = .004) and control bladder samples (14.55 ± 2.08, P = .004). The E-cadherin expression was also significantly decreased in IC/BPS bladder samples (59.05 ± 9.48) compared with the controls (96.30 ± 9.15, P = .001). No significant difference was found in E-cadherin or ZO-1 levels between the OAB and control bladders (P = .170 and P = .763, respectively). CONCLUSION: Mast cell infiltration was found in both OAB and IC/BPS bladder wall, but E-cadherin and ZO-1 expression was only decreased in IC/BPS, suggesting the urothelial barrier function was not affected in the OAB bladder.

[Blood lymphocytes and mast cells of the detrusor as diagnostic markers of overactive urinary bladder and its immune inflammation].

To identify clinico-laboratory symptoms and pathogenetic factors of overactive bladder syndrome (OBS), we used cytochemical analysis of peripheral blood lymphocyte enzymes in 88 males and females aged 50-75 years with this syndrome (70 patients) and control (18 subjects). Biopsy of the anterior wall of the bladder with examination of detrusor myocytes was made in 28 of 70 patients. OBS patients were found to have reduced aerobic respiration in blood lymphocytes and detruzor cells, dystrophy and atrophy of myocytes, moderate interstitial cell infiltration of the detrusor in increasing number and activity of mast cells, T-lymphocytes (CD4, CD8) and macrophages (CD11). We came to the conclusion that development and symptoms of OBS are caused by low energetic activity of the detrusor in line with dysfunction of the bladder mast cells and immunity factors. This is important for diagnosis of OBS severity and choice of energotropic therapeutic measures.