title: NLRP3 inflammasome may regulate inflammatory response of human periodontal ligament fibroblasts in an apoptosis-associated speck-like protein containing a CARD (ASC)-dependent manner.
abstract: OBJECTIVE
  To explore the role of NLRP3 (NACHT [nucleotide-binding oligomerization], LRR [leucine-rich repeat] and PYD [pyrin domain] domains-containing protein 3) inflammasome in the inflammatory response of human periodontal ligament fibroblasts (HPDLFs).
  
  
  METHODS
  The expression of NLRP3 and apoptosis-associated speck-like protein containing a CARD (ASC) in inflammatory periapical tissues and HPDLFs was examined by immunohistochemical and immunofluorescent staining. HPDLFs were stimulated with muramyl dipeptide (MDP) and lipopolysaccharide (LPS) from E. coli with or without the silencing of ASC. The expression of NLRP3, ASC and caspase-1 was examined using quantitative real-time polymerase chain reaction. The secretion of proinflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) was measured in the cell supernatant with an enzyme-linked immunosorbent assay. Data were statistically analysed using independent sample t-tests.
  
  
  RESULTS
  Immunohistochemistry and immunocytochemistry staining revealed that NLRP3 and ASC were expressed in HPDLFs and inflammatory periapical tissues. MDP and LPS promoted the expression of NLRP3, ASC and caspase-1 in HPDLFs (P < 0.05). The secretion of proinflammatory cytokines was also increased with MDP and LPS stimulation (P < 0.05). After silencing ASC, the secretion of IL-1β induced by MDP and LPS was significantly attenuated (P < 0.05).
  
  
  CONCLUSIONS
  In HPDLFs, MDP and LPS activated NLRP3 inflammasome and induced IL-1β secretion. ASC plays an important role in this inflammatory response.
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.|Department of Conservative Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: W L
authors.initials: WL
authors.lastname: Lu
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.|Department of Conservative Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: D Z
authors.initials: DZ
authors.lastname: Song
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.|Department of Conservative Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: J L
authors.initials: JL
authors.lastname: Yue
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: T T
authors.initials: TT
authors.lastname: Wang
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.|Department of Conservative Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: X D
authors.initials: XD
authors.lastname: Zhou
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.|Department of Conservative Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: P
authors.initials: P
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.|Department of Conservative Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: L
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.|Department of Conservative Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
authors.forename: D M
authors.initials: DM
authors.lastname: Huang
mesh_terms: D017209:Apoptosis; D053468:CARD Signaling Adaptor Proteins / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism*; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000378:metabolism*; D010513:Periodontal Ligament / Q000166:cytology* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053468:CARD Signaling Adaptor Proteins; D058847:Inflammasomes; D053583:Interleukin-1beta; D015850:Interleukin-6; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human; C402202:PYCARD protein, human; D014409:Tumor Necrosis Factor-alpha
keywords: 
  ASC
  ; NLRP3; human periodontal ligament fibroblasts; inflammasome; inflammation