XXXX b-defensin-2 may regulate the effect of bacillus Calmette-Gu  rin (BCG) in normal @entity19 bladder.

@entity19 @entity4 @entity30611 @entity16821
PURPOSE: We investigated whether bacillus Calmette-Gu  rin (BCG)-induced secretion of @entity19 b-defensin-2 ( @entity30611 ) and determined whether @entity30611 regulated BCG effects in the normal @entity19 bladder. MATERIALS AND METHODS: A total of 140 C57BL/6 female @entity19 were divided into 28 groups, and the experiment was performed over 3 steps. In the first step (20 groups), @entity19 bladders were stimulated with different doses of BCG (multiplicity of infection [MOI] 0, 1, 10, 30, and 100) and histological analysis was conducted in bladder specimens isolated at different times (0, 4, 8, and 24h after instillation) to determine optimal dose and time point of BCG internalization and urine @entity30611 and cytokine concentration. In the second step (4 groups), BCG internalization and urine cytokine levels were measured after pretreatment of different recombinant @entity30611 (rmBD2) (0, 1, 2.5, and 5ng/ml) at optimal dose and time point. In the third step (4 groups), BCG internalization and urine cytokine levels were compared between pretreatment conditions (control, rmBD2, anti- @entity30611 Ab, and rmBD2+anti- @entity30611 Ab). Urine was collected for estimating @entity30611 levels and a multiplex analysis for 9 cytokines. Real-time polymerase chain reaction assay was used for estimating the relative BCG cell number in @entity19 bladder tissue. RESULTS: Bladder @entity4 was induced by BCG (MOI 30 and 100), which progressed to an inflammatory infiltrate composed primarily of neutrophils and increased @entity30611 secretion at 4 hours after instillation. Relative BCG cell number and urinary cytokine levels (interferon-y and interleukins [IL]-2, -4, -6, and -10) response pattern was characterized by a peak at 4 hours after instillation followed by rapid decline. The levels of interferon-y, and @entity16821 and relative BCG cell numbers decreased in a dose-dependent manner according to pretreatment with rmBD2 protein, and the responses were potentiated in the anti- @entity30611 pretreatment group at 4 hours after BCG (MOI 30) instillation. CONCLUSION: The present results suggest that the @entity19 urothelium produces @entity30611 in response to intravesicular BCG as a defense mechanism against BCG, and blocking @entity30611 by an anti- @entity30611 antibody increased the effectiveness of BCG.
