Urinary tract infection is one of the most common bacterial infections and can cause major burdens, not only to individuals but also to an entire society. Current knowledge of the microbial communities in the urinary tract has increased exponentially due to next-generation sequencing and expanded quantitative urine culture. We now acknowledge a dynamic urinary tract microbiome that we once thought was sterile. Taxonomic studies have identified the normal core microbiota of the urinary tract, and studies on the changes in microbiome due to sexuality and age have set the foundation for microbiome studies in pathologic states. Urinary tract infection is not only caused by invading uropathogenic bacteria but also by changes to the uromicrobiome milieu, and interactions with other microbial communities can also contribute. Recent studies have provided insights into the pathogenesis of recurrent urinary tract infections and antimicrobial resistance. New therapeutic options for urinary tract infections also show promise; however, further research is needed to fully understand the implications of the urinary microbiome in urinary tract infections.

Lee S, et al. J Korean Med Sci. 2021 May;36(20):e135. https://doi.org/10.3346/jkms.2021.36.e135

Yeo JK, et al. World J Mens Health. 2018 Jan;36:e1. https://doi.org/10.5534/wjmh.17030

Choi CI, et al. Investig Clin Urol. 2024 Mar;65(2):108-114. https://doi.org/10.4111/icu.20230385

Background and objectives: The aim of our study was to evaluate the role of diabetes mellitus (DM) as a significant factor affecting spontaneous stone expulsion, as suggested by previous research. Materials and methods: We investigated the influence of DM on the ureter using a murine model. The mouse-model arm of this study used 20 15 -week-old mice, including 10 normal (control) mice and 10 DM mice. We measured the proximal, middle and distal ureteral smooth muscle thickness in each mouse and the differences among ureteral sections were analyzed. Mouse ureteral specimens were also analyzed via western blotting to detect relative protein expression of phosphor–extracellular signal regulated kinases (P–ERK), phosphor–C–Jun N–terminal kinase (P–JNK), vascular endothelial growth factor (VEGF), and protein kinase C (PKC), which are representative factors involved in cell regulation. Results: We observed significant hyperproliferation of ureteral smooth muscle in DM mice compared to normal mice, which may provoke reduced peristalsis. The ureteral smooth muscle of DM mice was significantly thicker than that of normal mice in all ureteral tissues: proximal (p = 0.040), mid (p = 0.010), and distal (p = 0.028). The relative protein expression of P-ERK (p = 0.005) and P–JNK (p = 0.001) was higher in the diabetic group compared to the normal group. Additionally, protein expression of VEGF (p = 0.002) and PKC (p = 0.001) were remarkably up-regulated in DM mice. Conclusions: Hyperproliferation of ureteral smooth muscle was observed in DM mice, but not in normal mice. The pathways mediated by P–ERK, P–JNK, VEGF, and PKC may play an important role in pathological ureteral conditions.

Choi C, et al. Investig Clin Urol. 2026 Mar;67(2):123-130. https://doi.org/10.4111/icu.20250656