固有免疫分子NLRP3炎性小体在慢性细菌性前列腺炎中的作用

Role of the innate immune molecule NLRP3 inflammasome in chronic bacterial prostatitis

目的探讨固有免疫分子NOD样受体蛋白3(NLRP3)炎性小体在慢性细菌性前列腺炎(CBP)中的作用。方法选取2016年2月～2017年12月右江民族医学院附属医院(以下简称"我院")泌尿外科收治的120例CBP患者为研究对象,同时选取我院同期进行体检的60名健康者为对照组。CBP患者采用三甲氧苄氨嘧啶配合磺胺甲恶唑治疗,持续12周。采用慢性前列腺炎症状评分量表、前列腺常规检查评估CBP患者治疗效果,酶联免疫吸附试验测定CBP患者NLRP3及其下游调控因子白细胞介素1β(IL-1β)和IL-18的表达。结果治疗前CBP患者NLRP3炎性小体含量显著高于对照组(P <0.001);根据CBP患者NLRP3炎性小体含量的中位数为分界值,将患者分为高NLRP3组和低NLRP3组(每组各60例)。治疗后,低NLRP3组患者慢性前列腺炎症状评分(NIHCPSI)量表疼痛、排尿、生存质量评分和总分值降低程度明显大于高NLRP3组(P <0.05),临床治疗有效率显著高于高NLRP3组(P <0.05)。治疗前,两组患者NLRP3、IL-1β和IL-18含量均显著高于对照组(P <0.05),治疗后,两组患者上述指标显著降低,而且低NLRP3组患者降低幅度明显大于高NLRP3组(P <0.05)。治疗后两组患者前列腺液白细胞和卵磷脂小体计数比较,差异无统计学意义(P> 0.05),且两组受试对象在治疗过程中均未出现严重的不良反应。结论 NLRP3炎性小体含量改变是影响CBP治疗效果的潜在因素,靶向调控NLRP3炎性小体水平有助于提高CBP的临床疗效。

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.