[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.