Role of the innate immune molecule NLRP3 inflammasome in chronic bacterial prostatitis
HE Tao1 HUANG Huawu1 ZENG Yonglong2 GUO Ziwei2 XIE Qiuyu2
1.Inspection Institute, Youjiang Medical College for Nationalities, Guangxi Zhuang Autonomous Region, Baise 533000, China;
2.Department of Urology, Affiliated Hospital of Youjiang Medical College for Nationalities, Guangxi Zhuang Autonomous Region, Baise 533000, China
Abstract:Objective To investigate the role of the innate immune molecule NLRP3 inflammasome in chronic bacterial prostatitis (CBP). Methods The 120 cases of CBP patients who admitted to Department of Urology, Affiliated Hospital of Youjiang Medical College (hereinafter referred to as "our hospital") for Nationalities were selected as the research objects from February 2016 to December 2017. The 60 healthy subjects in the same period in our hospital were selected as the control group. CBP patients were treated with trimethoprim plus sulfamethoxazole for 12 weeks. The chronic prostatitis symptom score scale (NIH-CPSI) and routine prostate test were used to evaluate the therapeutic effects of CBP patients. The expression of NLRP3 and its downstream regulatory elements interleukin 1β (IL-1β) and IL-18 were measured by enzyme linked immunosorbent assay in CBP patients. Results Before treatment, the content of NLRP3 inflammatory corpuscule in CBP patients was significantly higher than that in the control group (P < 0.001). Patients were divided into high NLRP3 group and low NLRP3 group (60 cases in each group) according to the median NLRP3 inflammatory body content in CBP patients as the cut-off value. After treatment, pain, urination, quality of life scores and total scores of NIH-CPSI in low NLRP3 group were significantly superior than those in high NLRP3 group (P < 0.05). The clinical response rate of low NLRP3 group was higher than that of high NLRP3 group (P < 0.05). Before treatment, the levels of NLRP3, IL-1β and IL-18 in both groups were significantly higher than those in healthy subjects (P < 0.05). After treatment, the above indexes were significantly decreased in both groups, and the reduction in low NLRP3 group were significantly greater than high NLRP3 group (P < 0.05). After treatment, there was no significant difference in leukocyte and lecithin counts between the two groups (P > 0.05), and no significant adverse reactions were observed in both groups during the treatment. Conclusion The change of NLRP3 inflammasome content is a potential factor that affects the therapeutic effect of CBP. Targeting the NLRP3 inflammasome level can improve the clinical efficacy of CBP.