Inflammasomes and their regulation in periodontal disease: a review

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Inflammasomes and their regulation in periodontal disease : a review. / Aral, Kübra; Milward, Michael; Kapila, Yvonne; Berdeli, Afig; Cooper, Paul.

In: Journal of Periodontal Research, 20.01.2020.

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@article{87b6877efde645f59ed61c24b80a084a,
title = "Inflammasomes and their regulation in periodontal disease: a review",
abstract = "Interleukin‐1β (IL‐1β), which is secreted by host tissues leading to periodontal tissue inflammation, is a major pro‐inflammatory cytokine in the pathogenesis of periodontal disease. The conversion of pro‐IL‐1β into its biologically active form is controlled by multiprotein complexes named as inflammasomes, which are key regulator of host defense mechanisms and inflammasome involved diseases, including the periodontal diseases. Inflammasomes are regulated by different proteins and processes, including pyrin domain (PYD)‐only proteins (POPs), CARD‐only proteins (COPs), tripartite motif family proteins (TRIMs), autophagy, and interferons. A review of in vitro, in vivo, and clinical data from these publications revealed that several inflammasomes including (NOD)‐like receptor (NLR) pyrin domain‐containing 3 (NLRP3) and absent in melanoma 2 (AIM2) have been found to be involved in periodontal disease pathogenesis. To the best of our knowledge, the current article provides the first review of the literature focusing on studies that evaluated both inflammasomes and their regulators in periodontal disease. An upregulation for inflammasomes and a downregulation of inflammasome regulator proteins including POPs, COPs, and TRIMs have been reported in periodontal disease. Although interferons (types I and II) and autophagy have been found to be involved in periodontal disease, their possible role in inflammasome activation has not evaluated yet. Modulating the excessive inflammatory response by the use of inflammasome regulators may have potential in the management of periodontal disease.",
keywords = "autophagy, caspase activation and recruitment domains, inflammasomes, interferons, periodontal disease, pyrin domain, tripartite motif proteins",
author = "K{\"u}bra Aral and Michael Milward and Yvonne Kapila and Afig Berdeli and Paul Cooper",
year = "2020",
month = jan,
day = "20",
doi = "10.1111/jre.12733",
language = "English",
journal = "Journal of Periodontal Research",
issn = "0022-3484",
publisher = "Wiley",

}

RIS

TY - JOUR

T1 - Inflammasomes and their regulation in periodontal disease

T2 - a review

AU - Aral, Kübra

AU - Milward, Michael

AU - Kapila, Yvonne

AU - Berdeli, Afig

AU - Cooper, Paul

PY - 2020/1/20

Y1 - 2020/1/20

N2 - Interleukin‐1β (IL‐1β), which is secreted by host tissues leading to periodontal tissue inflammation, is a major pro‐inflammatory cytokine in the pathogenesis of periodontal disease. The conversion of pro‐IL‐1β into its biologically active form is controlled by multiprotein complexes named as inflammasomes, which are key regulator of host defense mechanisms and inflammasome involved diseases, including the periodontal diseases. Inflammasomes are regulated by different proteins and processes, including pyrin domain (PYD)‐only proteins (POPs), CARD‐only proteins (COPs), tripartite motif family proteins (TRIMs), autophagy, and interferons. A review of in vitro, in vivo, and clinical data from these publications revealed that several inflammasomes including (NOD)‐like receptor (NLR) pyrin domain‐containing 3 (NLRP3) and absent in melanoma 2 (AIM2) have been found to be involved in periodontal disease pathogenesis. To the best of our knowledge, the current article provides the first review of the literature focusing on studies that evaluated both inflammasomes and their regulators in periodontal disease. An upregulation for inflammasomes and a downregulation of inflammasome regulator proteins including POPs, COPs, and TRIMs have been reported in periodontal disease. Although interferons (types I and II) and autophagy have been found to be involved in periodontal disease, their possible role in inflammasome activation has not evaluated yet. Modulating the excessive inflammatory response by the use of inflammasome regulators may have potential in the management of periodontal disease.

AB - Interleukin‐1β (IL‐1β), which is secreted by host tissues leading to periodontal tissue inflammation, is a major pro‐inflammatory cytokine in the pathogenesis of periodontal disease. The conversion of pro‐IL‐1β into its biologically active form is controlled by multiprotein complexes named as inflammasomes, which are key regulator of host defense mechanisms and inflammasome involved diseases, including the periodontal diseases. Inflammasomes are regulated by different proteins and processes, including pyrin domain (PYD)‐only proteins (POPs), CARD‐only proteins (COPs), tripartite motif family proteins (TRIMs), autophagy, and interferons. A review of in vitro, in vivo, and clinical data from these publications revealed that several inflammasomes including (NOD)‐like receptor (NLR) pyrin domain‐containing 3 (NLRP3) and absent in melanoma 2 (AIM2) have been found to be involved in periodontal disease pathogenesis. To the best of our knowledge, the current article provides the first review of the literature focusing on studies that evaluated both inflammasomes and their regulators in periodontal disease. An upregulation for inflammasomes and a downregulation of inflammasome regulator proteins including POPs, COPs, and TRIMs have been reported in periodontal disease. Although interferons (types I and II) and autophagy have been found to be involved in periodontal disease, their possible role in inflammasome activation has not evaluated yet. Modulating the excessive inflammatory response by the use of inflammasome regulators may have potential in the management of periodontal disease.

KW - autophagy

KW - caspase activation and recruitment domains

KW - inflammasomes

KW - interferons

KW - periodontal disease

KW - pyrin domain

KW - tripartite motif proteins

U2 - 10.1111/jre.12733

DO - 10.1111/jre.12733

M3 - Review article

JO - Journal of Periodontal Research

JF - Journal of Periodontal Research

SN - 0022-3484

ER -