Granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is released by female mouse bladder urothelial cells and expressed by the urothelium as an early response to lipopolysaccharides (LPS)

Abstract

Urothelium and mBUC secreted GM-CSF as an early response to LPS. GM-CSF mediated downstream expression of VEGF and COX-2. Urothelial GM-CSF may function as a signaling mediator for both inflammation and pain transduction. Neurourol. Urodynam. 36:1020-1025, 2017. © 2016 Wiley Periodicals, Inc.

Urothelial MaxiK-activity regulates mucosal and detrusor metabolism

“…However, the changes in metabolism of mucosa and detrusor are significantly different, supporting previous work that different compartments of the bladder should be considered as separate entities [ 11 ]. Overall our work supports a growing body of evidence that the urothelium plays an important regulatory role in overall bladder function, not only in mediating solute transport, but also in sensing and communicating to other tissues, primarily the detrusor, to respond to bladder fullness [ 18 ]. A primary signaling mechanism to initiate this response is believed to be the action of ATP on P2X3 receptors of sensory nerves [ 19 , 20 ].…”

Non-histone nuclear protein HMGN2 differently regulates the urothelium barrier function by altering expression of antimicrobial peptides and tight junction protein genes in UPEC J96-infected bladder epithelial cell monolayer

“…Besides these components, urothelia also participate in maintaining the intrinsic barrier function through lipopolysaccharide (LPS)-mediated TLR4 signaling (Schilling et al, 2003). As a result, a variety of secreted proteins involved in inflammatory responses, including IL-8, IL-6 (Billips et al, 2007), GM-CSF (Li et al, 2017) and antibacterial mucosal proteins, such as the Surfactant Protein A (Hashimoto et al, 2017), are expressed. Therefore, like in the case of epithelium lining other parts of the body, invading pathogens can cross the urothelial barrier through intracellular tight and adherent junctions (paracellular route) or pass the apical surface of epithelial cells (transcellular route) (Balkovetz & Katz, 2003).…”

Mouse urothelial genes associated with voiding behavior changes after ovariectomy and bladder lipopolysaccharide exposure

“…Bladder urothelial cellular functions are altered in OAB, including augmented TRPV1, muscarinic M3 receptor, and VEGF signaling . The urothelial cells participate in the innate immune response secondary to LPS stimulus by releasing cytokines such as IL‐8 and GM‐CSF . Estrogen is a host defense factor that protects against cystitis from UTI through urothelial production of antimicrobial peptides mediated by estrogen receptor β .…”

“…[13][14][15] The urothelial cells participate in the innate immune response secondary to LPS stimulus by releasing cytokines such as IL-8 16 and GM-CSF. 17 Estrogen is a host defense factor that protects against cystitis from UTI through urothelial production of antimicrobial peptides mediated by estrogen receptor β. 18 These data justify focusing on the bladder urothelium to better understand host response in the context of menopause and bacterial exposure.…”