固有免疫分子NLRP3炎性小體在慢性細菌性前列腺炎中的作用

何濤 黃華武 曾永龍

[摘要] 目的 探討固有免疫分子NOD樣受體蛋白3（NLRP3）炎性小體在慢性細菌性前列腺炎（CBP）中的作用。方法 選取2016年2月～2017年12月右江民族醫(yī)學院附屬醫(yī)院（以下簡稱“我院”）泌尿外科收治的120例CBP患者為研究對象，同時選取我院同期進行體檢的60名健康者為對照組。CBP患者采用三甲氧芐氨嘧啶配合磺胺甲惡唑治療，持續(xù)12周。采用慢性前列腺炎癥狀評分量表、前列腺常規(guī)檢查評估CBP患者治療效果，酶聯(lián)免疫吸附試驗測定CBP患者NLRP3及其下游調控因子白細胞介素1β（IL-1β）和IL-18的表達。 結果 治療前CBP患者NLRP3炎性小體含量顯著高于對照組（P < 0.001）；根據(jù)CBP患者NLRP3炎性小體含量的中位數(shù)為分界值，將患者分為高NLRP3組和低NLRP3組（每組各60例）。治療后，低NLRP3組患者慢性前列腺炎癥狀評分（NIH-CPSI）量表疼痛、排尿、生存質量評分和總分值降低程度明顯大于高NLRP3組（P < 0.05），臨床治療有效率顯著高于高NLRP3組（P < 0.05）。治療前，兩組患者NLRP3、IL-1β和IL-18含量均顯著高于對照組（P < 0.05），治療后，兩組患者上述指標顯著降低，而且低NLRP3組患者降低幅度明顯大于高NLRP3組（P < 0.05）。治療后兩組患者前列腺液白細胞和卵磷脂小體計數(shù)比較，差異無統(tǒng)計學意義（P > 0.05），且兩組受試對象在治療過程中均未出現(xiàn)嚴重的不良反應。 結論 NLRP3炎性小體含量改變是影響CBP治療效果的潛在因素，靶向調控NLRP3炎性小體水平有助于提高CBP的臨床療效。

[關鍵詞] 慢性細菌性前列腺炎；NOD樣受體蛋白3；炎性小體

[中圖分類號] R697 [文獻標識碼] A [文章編號] 1673-7210（2019）04（a）-0157-05

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.