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Background: The incidence of urinary tract infections (UTIs) after radical cystectomy (RC) with urinary diversion (UD), the typical pathogens, and associated patient risk factors have not been well documented. In this study, we examined the incidence of post-op UTIs after RC to identify associated risk factors. Methods: Single-center, retrospective case series of 386 patients with bladder cancer who underwent RC with UD between 2012 and 2024. The primary objective was UTI incidence, defined by the frequency of patients with urine culture with >105 colony-forming units per high-powered field, spanning from post-op day 0 (POD0) to 90 days after discharge. Isolated pathogens were reported. Risk factors for UTIs were assessed. Results: The average age was 69 years old at surgery, and patients were predominantly male (80%). The cumulative incidence of post-op UTIs was 14%, among which 12 patients had more than one UTI. The UTI incidence was 2%, 8%, and 7% during the immediate post-op period, within 30 days, and within 31–90 days, respectively. Isolated pathogens included Escherichia coli (26%), Enterococcus faecalis (24%), Klebsiella pneumoniae (21%), and Pseudomonas species (21%). In the immediate post-op period, female sex was the only significant risk factor. At 31 to 90 days, cutaneous ureterostomy UD was the predominant risk factor for UTIs. For ileal conduit patients, those with a Wallace ureteral anastomosis were associated with UTI 31–90 days from discharge for RC. Conclusions: Our retrospective data suggests the incidence of UTIs and their causative pathogens after RC differ based on post-operative time points and vary according to different patient risk factors. [ABSTRACT FROM AUTHOR]

The cytokines of the transforming growth factor-β (TGF-β) family promote the growth and differentiation of multiple tissues, but the role of only the founding member, TGF-β, in regulating the immune responses has been extensively studied. TGF-β is critical to prevent the spontaneous activation of self-reactive T cells and sustain immune homeostasis. In contrast, in the presence of proinflammatory cytokines, TGF-β promotes the differentiation of effector T helper 17 (TH17) cells. Abrogating TGF-β receptor signaling prevents the development of interleukin-17 (IL-17)- secreting cells and protects mice from TH17 cell-mediated autoimmunity. We found that the receptor of another member of TGF-β family, bone morphogenetic protein receptor 1α (BMPR1α), regulates T helper cell activation. We found that the differentiation of TH17 cells from naive CD4+ T cells was inhibited in the presence of BMPs. Abrogation of BMPR1α signaling during CD4+ T cell activation induced a developmental program that led to the generation of inflammatory effector cells expressing large amounts of IL-17, IFN-γ, and TNF family cytokines and transcription factors defining the TH17 cell lineage. We found that TGF-β and BMPs cooperated to establish effector cell functions and the cytokine profile of activated CD4+ T cells. Together, our data provide insight into the immunoregulatory function of BMPs. [ABSTRACT FROM AUTHOR]