Influence of inflammasome NLRP3, and IL1B and IL2 gene polymorphisms in periodontitis susceptibility

Alencar, Josiane Bazzo de; Zacarias, Joana Maira Valentini; Tsuneto, Patrícia Yumeko; Souza, Victor Hugo de; Silva, Cléverson O.; Visentainer, Jeane Eliete Laguila; Sell, Ana Maria

doi:10.1371/journal.pone.0227905

Cited by 30 publications

(17 citation statements)

References 88 publications

(105 reference statements)

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“…IL16 polymorphisms were previously studied in PD [23,24]. Other SNPs in cytokine genes such as IL-1β, IL-2, IL-17 and IL-18 were associated with PD in our population from southern Brazil [25][26][27].…”

Section: Introductionmentioning

confidence: 85%

Association of IL16 polymorphisms with periodontitis in Brazilians: A case- control study

et al. 2020

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Periodontitis (PD) is a chronic inflammatory process resulting from the relationship of the immune response with the components in dental plaque. Cytokines and their genetic polymorphisms seem to be involved in the immunopathogenesis of this disease. This study aimed to evaluate the correlation of IL16 polymorphism with PD. A case-control study was conducted in a sample of individuals from southern Brazil. The genotyping of IL16, rs11556218 T>G, rs4072111 C>T e rs4778889 T>C, was performed using the PCR-RFLP methodology. The serum level of IL-16 was determined using an IL-16 ELISA kit for humans. SNPStats and OpenEpi software and Wilcoxon's U test were used to perform statistical analysis. IL16 rs11556218 polymorphism was significantly associated to PD in nonsmoking patients: individuals with G/G genotype were less likely to develop PD compared to the T/T genotype (OR = 0.10; Pc = 0.019, codominant model). In addition, the TTT haplotype was associated with a high risk for PD (OR = 2.45; P = 0.01). A low IL-16 serum level was observed among individuals with PD when compared to controls (P = 0.027). Thus, the IL16 rs16556218 polymorphism and the serum levels of IL-16 were associated with periodontitis in a Brazilian sample, and this was influenced by environmental factors such as smoking.

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Section: Introductionmentioning

confidence: 85%

Association of IL16 polymorphisms with periodontitis in Brazilians: A case- control study

et al. 2020

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“…1,6 Additionally, inflammasome polymorphisms were recently shown to put men at greater risk for developing periodontitis. 25 Further understanding of the role of the inflammasome in disease pathogenesis will help lead to precision care. Based on our knowledge thus far, individuals within the Socransky trait may benefit by adjunct therapeutic inhibition of the inflammasome to treat periodontitis.…”

Section: Inflammasomes In Periodontal Diseasementioning

confidence: 99%

“…Evidence supporting the predisposition of groups of individuals to develop periodontitis is evolving 1,6 . Additionally, inflammasome polymorphisms were recently shown to put men at greater risk for developing periodontitis 25 . Further understanding of the role of the inflammasome in disease pathogenesis will help lead to precision care.…”

Section: Inflammasomes In Periodontal Diseasementioning

confidence: 99%

Inflammasomes as contributors to periodontal disease

Marchesan

2020

Journal of Periodontology

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A genome-wide association study of ≈2.5 million markers identified unique biologically informed periodontal complex traits with distinct microbial communities and interleukin-1β (IL-1β) levels. Each trait was associated with different single nucleotide polymorphisms. These variants include genes associated with immune responses, microbial colonization, and the epithelial barrier function. The specific set of variants leads to individual biological paths that converge into an overlapping clinical phenotype of periodontal tissue destruction. This concept suggests that periodontal disease is a group of distinct conditions. We identified polymorphisms in inflammasome genes interferon gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) that were associated with increased severity of periodontal disease. Inflammasomes respond to pathogen or tissue "danger" signals and assemble into multiprotein "machineries" that are essential for the cleavage of proinflammatory mediator IL-1β into an active form. Thus, understanding how variants of IFI16 and AIM2 contribute to periodontal disease pathogenesis may lead to treatment options that address individual biological variations and precision therapies for oral health.

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“…Studies have demonstrated that NLRP3 activation increases adipogenesis and inhibits the osteogenesis of human umbilical cord stem cells, while the silencing of NLRP3 alleviates estrogen depletion-induced osteoporosis in mice ( 18 , 19 ). Most importantly, previous clinical studies have reported that gene polymorphisms of NLRP3 are associated with susceptibility to periodontitis and the expression levels of NLRP3 inflammasome-associated proteins are particularly enhanced in periodontitis ( 20 , 21 ). However, whether NLRP3 associates with NF-κB to inhibit the osteogenic differentiation of hPDLSCs needs to be elucidated in a model of TNF-α-induced periodontitis.…”

Section: Introductionmentioning

confidence: 99%

Quercetin reverses TNF‑α induced osteogenic damage to human periodontal ligament stem cells by suppressing the NF‑κB/NLRP3 inflammasome pathway

et al. 2021

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Quercetin (Quer) is a typical antioxidant flavonoid from plants that is involved in bone metabolism, as well as in the progression of inflammatory diseases. Elevated levels of tumor necrosis factor-α (TNF-α), a typical pro-inflammatory cytokine, can affect osteogenesis. In the present study, TNF-α was used to establish an in vitro model of periodontitis. The effects of Quer on, as well as its potential role in the osteogenic response of human periodontal ligament stem cells (hPDLSCs) under TNF-α-induced inflammatory conditions and the underlying mechanisms were then investigated. Within the appropriate concentration range, Quer did not exhibit any cytotoxicity. More importantly, Quer significantly attenuated the TNF-α induced the suppression of osteogenesis-related genes and proteins, alkaline phosphatase (ALP) activity and mineralized matrix in the hPDLSCs. These findings were associated with the fact that Quer inhibited the activation of the NF-κB signaling pathway, as well as the expression of NLRP3 inflammation-associated proteins in the inflammatory microenvironment. Moreover, the silencing of NLRP3 by small interfering RNA (siRNA) was found to protect the hPDLSCs against TNF-α-induced osteogenic damage, which was in accordance with the effects of Quer. On the whole, the present study demonstrates that Quer reduces the impaired osteogenesis of hPDLSCs under TNF-α-induced inflammatory conditions by inhibiting the NF-κB/NLRP3 inflammasome pathway. Thus, Quer may prove to be a potential remedy against periodontal bone defects.

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Influence of inflammasome NLRP3, and IL1B and IL2 gene polymorphisms in periodontitis susceptibility

Cited by 30 publications

References 88 publications

Association of IL16 polymorphisms with periodontitis in Brazilians: A case- control study

Association of IL16 polymorphisms with periodontitis in Brazilians: A case- control study

Inflammasomes as contributors to periodontal disease

Quercetin reverses TNF‑α induced osteogenic damage to human periodontal ligament stem cells by suppressing the NF‑κB/NLRP3 inflammasome pathway

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