Cystitis Induces Altered CREB Expression Related with Micturition Reflex

Background and objectives: Bladder stimulation upregulates neurotrophins associated with voiding reflex. Bacterial cystitis can be a stimulant that activates this system, resulting in a pathological state. Phosphorylated responsive element of binding protein (p-CREB) is a pivotal transcriptional factor in the neurotrophin signaling cascade. The goal of our study was to examine the change in expression of p-CREB in dorsal root ganglia (DRG) of rats after uropathogenic Escherichia coli infection of the bladder. Materials and methods: A total of 19 adult female Sprague−Dawley rats were induced with acute E. coli infection (n = 7), chronic E. coli infection (n = 6), or served as controls (n = 6). In each group, the profiles of p-CREB cell were counted in 6−10 sections of each of the DRG collected. DRG cells exhibiting intense nuclear staining were considered to be positive for p-CREB immunoreactivity (p-CREB-IR). Results: Overall, the immunoreactivity of p-CREB was examined in smaller cell profiles with nuclear staining or nuclear and cytoplasmic staining in the DRGs (L1−L6, S1). In the chronic cystitis group, p-CREB-IR in the L1−L6 and S1 DRG was significantly higher than the control group (p < 0.05). Further, p-CREB-IR in the L3−L6 and S1 DRG of the chronic cystitis group was significantly greater than that in the acute cystitis group (p < 0.05). In the control and acute cystitis groups, p-CREB-IR in the L4−L5 DRG was significantly lower than that found in the other DRG sections (p < 0.05). Conclusions: Altogether, acute or chronic E.coli cystitis changed the immunoreactivity of p-CREB in lumbosacral DRG cells. In particular, chronic E. coli infection triggered p-CREB overexpression in L1−L6 and S1 DRG, indicating subsequent pathologic changes.