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Introduction:The host response to bacterial cystitis (UTI) has been poorly studied. It has been suggested that IL-6 and IL-8 were released by different types of cultured BUC in response to infections. We studied freshly cultured mBUC and cytokine release in response to LPS exposure as a surrogate of bacterial infection.
Materials & Methods:mBUC from C57BL/6 mice were grown in culture using published techniques and used within 3 days. LPS at 100 ng/ml, 1 μg/ml and 10 μg/ml were used. Supernatant was collected at 24 hours of LPS exposure and assayed using a multiplex ELISA for IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-17A, IFN-γ, TNF-α, G-CSF and GM-CSF. Splenic cell served as positive controls. Quantitative RT-PCR (q-RTPCR) for GM-CSF transcript was also performed.
Results:LPS induced mBUC to release negligible amounts of every cytokine tested, except for GM-CSF, where a 2-fold increase (normalized for protein content) was detected at the highest LPS dose (p<0.05 comparing to no LPS exposure). q-RTPCR showed a dose-response increase in GM-CSF transcript levels, such that at the highest LPS exposure, GM-CSF mRNA was 3.5-fold higher than the untreated control (with data normalized for α-actin transcript levels).
Conclusions:It was surprising that mBUC exposed to LPS released only GM-CSF, but this effect was significant. This is the first report of BUC releasing GM-CSF. This finding is significant because GM-CSF is an important mediator of pain pathways (GM-CSF is nociceptive). GM-CSF released by BUC may mediate UTI-related bladder pain, and possibly bladder pain in general unrelated to UTI.