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 32 publications

(20 citation statements)

References 88 publications

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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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“…Negative inflammasome regulators, such as POP1, POP2, and CARD18, are also downregulated in periodontitis, further indicating increased inflammasome activity ( 225 ). Polymorphisms in various inflammasome components, including NLRP3, AIM2, and IFI16, may be associated with susceptibility to periodontitis ( 226 – 229 ). The mRNA levels of murine Ifi204 , which has a structure and function similar to those of human IFI16 , were also increased in gingival tissues of ligature-induced periodontitis ( 230 ).…”

Section: Inflammasomes In Inflammatory Osteolysis Of the Alveolar Bone And Jawsmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

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

Cited by 32 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 in Alveolar Bone Loss

Inflammasomes as contributors to periodontal disease

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