[Effect of IL-1β and NLRP3 on the inflammatory response of acne vulgaris].

To investigate the pathogenesis of acne vulgaris, and to provide new ideas for non-antibiotic therapy for acne vulgaris. Methods: Normal human epidermal keratinocyte (NHEK) was exposed to Propionibacterium acnes (P. acnes) [multiplicity of infection (MOI)=10, 20, 30] for 12, 24, or 36 hours. The enzyme-linked immunosorbent assay (ELISA) and real-time PCR were used to detect the protein and mRNA of IL-1β in NHEK. Three groups were set up as follows: A negative control group (no NHEK pretreatment), a positive control group (P. acnes was used to stimulate NHEK), and a siRNA group (pretreated NHEK with siRNA). ELISA, real-time PCR, and Western blotting were used to detect the protein, mRNA of IL-1β and nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 (NLRP3) in NHEK. Results: IL-1β of NHEK in the positive control group was significantly increased in a time and dose-dependent manner compared with the negative control group (P<0.05). After pretreating NHEK with siRNA, IL-1β level was decreased compared with the positive control group, but it was higher than that in the negative control group (P<0.05). Conclusion: P. ances can stimulate NHEK to secrete IL-1β, and the process is possibly involved in NLRP3. The inflammatory response induced by P. ances could be inhibited by suppressing the activity of NLRP3.目的：探讨痤疮的发病机制，为痤疮的非抗生素治疗提供新思路。方法：分别使用感染复数(multiplicity of infection，MOI)为0，10，20，30的痤疮丙酸杆菌菌悬液刺激正常人表皮角质形成细胞(normal human epidermal keratinocyte，NHEK)12，24，36 h后，使用ELISA，real-time PCR检测NHEK中IL-1β的蛋白及mRNA的表达。另设3组：空白对照组，未进行任何预处理的NHEK；阳性对照组，仅使用MOI为30的痤疮丙酸杆菌菌悬液刺激NHEK；siRNA组，使用特异性小干扰RNA(siRNA)预处理以后再使用MOI为30的痤疮丙酸杆菌菌悬液刺激NHEK，使用蛋白质印迹法检测3组中NOD样受体蛋白3(nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3，NLRP3)炎性小体的表达情况，使用ELISA，real-time PCR检测3组NHEK中IL-1β蛋白及mRNA的表达。结果：不同浓度痤疮丙酸杆菌菌悬液刺激NHEK后，IL-1β表达量较空白对照组均有不同程度的升高，升高程度呈时间及剂量相关性(P<0.05)。siRNA预处理NHEK后，NLRP3炎性小体以及IL-1β的表达量明显降低，但仍高于空白对照组(P<0.05)。结论：痤疮丙酸杆菌刺激NHEK分泌IL-1β可能需要NLRP3炎性小体的参与；可通过抑制NLRP3炎性小体的活性来抑制由痤疮丙酸杆菌导致的炎性反应，从而减少抗生素的使用。.