Kübra Aral1, Eynar Berdeli2, Paul Roy Cooper3, Michael Robert Milward3, Yvonne Kapila4, Beyza Karadede Ünal2, Cüneyt Asım Aral5, Afig Berdeli6. 1. Oral Biology, School of Dentistry, University of Birmingham, Birmingham, UK. 2. Faculty of Dentistry, Izmir Katip Celebi University, Izmir, Turkey. 3. School of Dentistry, University of Birmingham, Birmingham, UK. 4. The School of Dentistry, University of California San Francisco, San Francisco, CA, USA. 5. Faculty of Dentistry, Inonu University, Malatya, Turkey. 6. Faculty of Medicine, Molecular Medicine Laboratory, Ege University, Izmir, Turkey.
Abstract
BACKGROUND: The inflammasome modulates the release of key proinflammatory cytokines associated with periodontal disease pathogenesis. The aim of this study was to evaluate the expression of proteins that regulate the inflammasome, namely pyrin domain-only proteins (POPs), caspase activation recruitment domain (CARD)-only proteins, and tripartite motif-containing (TRIM) proteins, in periodontal diseases. METHODS: A total of 68 participants (34 males and 34 females) were divided into four groups, including periodontal health (H), gingivitis (G), chronic periodontitis (CP), and aggressive periodontitis (AgP) based on clinical parameters. Gingival tissue samples were obtained from all participants for reverse transcription polymerase chain reaction (RT-PCR)-based gene expression analyses of molecules that regulate the inflammasome, including apoptosis-associated speck-like protein (ASC) containing CARD, caspase-1, interleukin-1β (IL-1β), interleukin-18 (IL-18), nucleotide-binding domain, leucine rich family (NLR) pyrin domain containing 3 (NLRP3), NLR family pyrin domain containing 2 (NLRP2), AIM2 (absent in melanoma 2), POP1, POP2, CARD16, CARD18, TRIM16, and TRIM20 by RT-PCR. RESULTS: NLRP3 and IL-1β were upregulated in the G, CP, and AgP groups compared with group H (P < 0.05). AIM2 was downregulated in the CP group compared with the H, G, and AgP groups (P < 0.05). TRIM20, TRIM16, and CARD18 were downregulated in the G, CP, and AgP groups compared with the H group (P < 0.05). POP1 and POP2 were downregulated in the CP and AgP, and AgP and G groups, respectively (P < 0.05). CONCLUSION: Active periodontal disease may result in downregulation of inflammasome regulators that may increase the activity of NLRP3 and IL-1β in periodontal disease.
BACKGROUND: The inflammasome modulates the release of key proinflammatory cytokines associated with periodontal disease pathogenesis. The aim of this study was to evaluate the expression of proteins that regulate the inflammasome, namely pyrin domain-only proteins (POPs), caspase activation recruitment domain (CARD)-only proteins, and tripartite motif-containing (TRIM) proteins, in periodontal diseases. METHODS: A total of 68 participants (34 males and 34 females) were divided into four groups, including periodontal health (H), gingivitis (G), chronic periodontitis (CP), and aggressive periodontitis (AgP) based on clinical parameters. Gingival tissue samples were obtained from all participants for reverse transcription polymerase chain reaction (RT-PCR)-based gene expression analyses of molecules that regulate the inflammasome, including apoptosis-associated speck-like protein (ASC) containing CARD, caspase-1, interleukin-1β (IL-1β), interleukin-18 (IL-18), nucleotide-binding domain, leucine rich family (NLR) pyrin domain containing 3 (NLRP3), NLR family pyrin domain containing 2 (NLRP2), AIM2 (absent in melanoma 2), POP1, POP2, CARD16, CARD18, TRIM16, and TRIM20 by RT-PCR. RESULTS: NLRP3 and IL-1β were upregulated in the G, CP, and AgP groups compared with group H (P < 0.05). AIM2 was downregulated in the CP group compared with the H, G, and AgP groups (P < 0.05). TRIM20, TRIM16, and CARD18 were downregulated in the G, CP, and AgP groups compared with the H group (P < 0.05). POP1 and POP2 were downregulated in the CP and AgP, and AgP and G groups, respectively (P < 0.05). CONCLUSION: Active periodontal disease may result in downregulation of inflammasome regulators that may increase the activity of NLRP3 and IL-1β in periodontal disease.
Authors: Josiane Bazzo de Alencar; Joana Maira Valentini Zacarias; Patrícia Yumeko Tsuneto; Victor Hugo de Souza; Cléverson de Oliveira E Silva; Jeane Eliete Laguila Visentainer; Ana Maria Sell Journal: PLoS One Date: 2020-01-24 Impact factor: 3.240