Effect of IL-1β and NLRP3 on the inflammatory response of acne vulgaris.
10.11817/j.issn.1672-7347.2019.04.011
- Author:
Xiaojuan LI
1
;
Xinyu LIN
1
;
Zhu SHEN
1
;
Qiu DENG
1
;
Ying LIU
1
;
Shi CHENG
1
Author Information
1. Department of Dermatology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu 610072, China.
- Publication Type:Journal Article
- MeSH:
Acne Vulgaris;
Humans;
Inflammasomes;
Interleukin-1beta;
Keratinocytes;
NLR Family, Pyrin Domain-Containing 3 Protein;
Propionibacterium acnes
- From:
Journal of Central South University(Medical Sciences)
2019;44(4):413-418
- CountryChina
- Language:Chinese
-
Abstract:
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.
