The Potential Role of Urinary Microbiome in Benign Prostate Hyperplasia/Lower Urinary Tract Symptoms

Abstract

Historically, urine in the urinary tract was considered “sterile” based primarily on culture-dependent methods of bacterial detection. Rapidly developing sequencing methods and analytical techniques have detected bacterial deoxyribonucleic acid and live bacteria in urine, improving our ability to understand the urinary tract microbiome. Recently, many studies have revealed evidence of a microbial presence in human urine in the absence of clinical infections. In women, fascinating evidence associates urinary tract microbiota with lower urinary tract symptoms (LUTS). However, the association between urinary tract microbiota and men with LUTS, particularly those with benign prostate hyperplasia (BPH), has not been established. In addition, the identification of the proinflammatory cytokines and pathogens responsible for the clinical progression of BPH is still underway. This review article aimed to address microbiome-related evidence for BPH. Further studies are required for a comprehensive understanding of the relationship between the urogenital microbiome and BPH pathogenesis to facilitate the development of preventive and therapeutic approaches for male LUTS.

Overview of BPH: Symptom Relief with Dietary Polyphenols, Vitamins and Phytochemicals by Nutraceutical Supplements with Implications to the Prostate Microbiome

“…The chronic inflammatory process: the link between the initial cause and the growth factor stimulated hyperplasia of glandular cellular proliferation seen in BPH is clear [ 12 ]. However, the initial stimulus for the inflammatory process is unknown; however, several potential factors may include bacterial or viral infections, hormone changes, dietary factors, autoimmune responses, urinary reflux into the prostate collecting ducts, and the potentially the prostate microbiome [ 10 , 12 , 26 , 27 ]. While there is some evidence that AR expression is elevated in certain cellular compartments, AR signaling within stromal cells alters intercellular signaling and changes in epithelial AR expression leads to paracrine signaling and/or chronic inflammation that further aids in stromal or epithelial proliferation in BPH [ 20 ].…”

The Urinary Microbiome; Axis Crosstalk and Short-Chain Fatty Acid

“…When inflammasome is activated, it induces proteolytic cleavage of pro-capsase1 to generate caspase-1. Inflammasomes can promote maturation and secretion of proinflammatory cytokines interleukin 1β (IL-1β) and interleukin 18 (IL-18) and promote pyroptosis programmed into proinflammatory cell death distinct from apoptosis [ 31 , 32 ]. Pyroptosis in turn releases ATP, uric acid, and intracellular damage-associated molecular patterns (DAMPs) that further propagates inflammation [ 32 ].…”

“…The NLRP3 inflammasome is located within the cell. It can recognize two types of signals: pathogen-associated molecular patterns (PAMPs) and DAMPs [ 31 , 33 ]. Inflammasomes are expressed in immune and non-immune cells, which contribute to the detection of pathogens and danger signals.…”

“…Additionally, the inhibition of NLRP3 with glyburide or IL-1β with a receptor antagonist (anakinra) blocked the appearance of fibrotic endpoints [ 45 ]. Eventually, benign prostate hyperplasia (BPH) could be a result of inflammasome activation [ 31 , 46 ].…”

Possibilities and limitations of using low biomass samples for urologic disease and microbiome research

“…Transurethral catheterization could be the most preferred sampling method which could gain similar outcomes less invasively compared to suprapubic aspiration. 98 , 99 …”