New therapy with ASC-J9® to suppress the prostatitis via altering the cytokine CCL2 signals

Abstract

Prostatitis is a common disease contributing to 8% of all urologist visits. Yet the etiology and effective treatment remain to be further elucidated. Using a non-obese diabetes mouse model that can be induced by autoimmune response for the spontaneous development of prostatitis, we found that injection of the ASC-J9^® at 75 mg/Kg body weight/48 hours led to significantly suppressed prostatitis that was accompanied with reduction of lymphocyte infiltration with reduced CD4⁺ T cells in prostate. In vitro studies with a co-culture system also confirmed that ASC-J9^® treatment could suppress the CD4⁺ T cell migration to prostate stromal cells. Mechanisms dissection indicated that ASC-J9^® can suppress CD4⁺ T cell migration via decreasing the cytokine CCL2 in vitro and in vivo, and restoring CCL2 could interrupt the ASC-J9^® suppressed CD4⁺ T cell migration. Together, results from in vivo and in vitro studies suggest that ASC-J9^® can suppress prostatitis by altering the autoimmune response induced by CD4⁺ T cell recruitment, and using ASC-J9^® may help us to develop a potential new therapy to battle the prostatitis with little side effects.