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      NLRP1 and NLRC4 inflammasomes are not responsible for the induction of inflammation in pulp tissues from carious teeth

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          Abstract

          Introduction:

          Inflammation is a risk factor for dental complications. Inflammasomes are a set of intracellular sensors which participate in the induction of inflammation. As the main factors involved in the induction of pulp inflammation in the carious teeth are yet to be clarified, this study was aimed to evaluate NLRP1 and NLRC4 expression levels in the inflamed and healthy pulps.

          Materials and Methods:

          Fifty inflamed and fifty healthy pulps were evaluated regarding the multiRNA levels of NLRP1 and NLRC4 using real-time polymerase chain reaction technique.

          Results:

          Results demonstrated that expression of NLRP1 ( P = 0.985) and NLRC4 ( P = 0.581) did not significantly differ in inflamed in comparison to healthy pulps. NLRP1 ( P = 0.989) and NLRC4 ( P = 0.170) did not change in males when compared with females in inflamed pulps. Furthermore, NLRP1 ( P = 0.133) and NLRC4 ( P = 0.642) were not altered in males in comparison to females in healthy pulps.

          Conclusion:

          Although NLRP1 and NLRC4 are the main inflammasomes, it appears that they are not the responsible molecules involved in the human pulp inflammation in the carious teeth.

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          Most cited references22

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          Beyond tissue injury-damage-associated molecular patterns, toll-like receptors, and inflammasomes also drive regeneration and fibrosis.

          Hans-Joachim Anders, Liliana Schaefer (2014)
          Tissue injury initiates an inflammatory response through the actions of immunostimulatory molecules referred to as damage-associated molecular patterns (DAMPs). DAMPs encompass a group of heterogenous molecules, including intracellular molecules released during cell necrosis and molecules involved in extracellular matrix remodeling such as hyaluronan, biglycan, and fibronectin. Kidney-specific DAMPs include crystals and uromodulin released by renal tubular damage. DAMPs trigger innate immunity by activating Toll-like receptors, purinergic receptors, or the NLRP3 inflammasome. However, recent evidence revealed that DAMPs also trigger re-epithelialization upon kidney injury and contribute to epithelial-mesenchymal transition and, potentially, to myofibroblast differentiation and proliferation. Thus, these discoveries suggest that DAMPs drive not only immune injury but also kidney regeneration and renal scarring. Here, we review the data from these studies and discuss the increasingly complex connection between DAMPs and kidney diseases. Copyright © 2014 by the American Society of Nephrology.
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            Mechanisms that lead to the regulation of NLRP3 inflammasome expression and activation in human dental pulp fibroblasts.

            Ansheng Zhang, Peina Wang, Xiaoying Ma … (2015)
            The NLRP3 inflammasome plays an important role in the cellular defense against invading pathogens and is reported to be expressed in human dental pulp fibroblasts (HDPFs). However, the role of the NLRP3 inflammasome in HDPFs during pulpal infection and inflammation remains unclear.
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              Activation of inflammasomes in adipose tissue of women with gestational diabetes.

              Martha Lappas (2014)
              Gestational diabetes mellitus (GDM) is characterised by maternal peripheral insulin resistance, increased inflammation, and increasing levels of circulating free fatty acids (FFAs) and advanced glycation endproducts (AGEs). Caspase-1 is a key component of the inflammasome, which is activated upon cellular infection or stress to trigger the maturation IL-1β, a pro-inflammatory cytokine that mediated insulin resistance. The aim of this study was to determine whether the inflammasome is activated in adipose tissue from women with gestational diabetes mellitus (GDM) and if it interferes with the insulin signalling pathway leading to the insulin resistance that is evident in GDM. Protein expression of active caspase-1 and mature IL-1β secretion was increased in adipose tissue of women with GDM. Treatment of adipose tissue with IL-1β decreased insulin-stimulated phosphorylation of IRS-1, GLUT-4 expression and glucose uptake. Low-grade inflammation (induced by LPS), the FFA palmitate and AGE conjugated to BSA (AGE-BSA), induced IL-1β secretion via inflammasome activation. In conclusion, the present findings describe an important role for adipose tissue inflammasome activation in the development of insulin resistance associated in pregnancies complicated by GDM. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Conserv Dent
                Journal ID (iso-abbrev): J Conserv Dent
                Journal ID (publisher-id): JCD
                Title: Journal of Conservative Dentistry : JCD
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 0972-0707
                ISSN (Electronic): 0974-5203
                Publication date (Print): Jan-Feb 2019
                Volume: 22
                Issue: 1
                Pages: 12-16
                Affiliations
                [1 ]Department of Endodontics, Faculty of Dental Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
                [2 ]Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
                Author notes
                Address for correspondence: Dr. Mohammad Mahdi Yaghooti Khorasani, Department of Endodontics, Faculty of Dental Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. E-mail: m.yaghooti@ 123456yahoo.com
                Article
                Publisher ID: JCD-22-12
                DOI: 10.4103/JCD.JCD_195_18
                PMC ID: 6385575
                PubMed ID: 30820076
                SO-VID: 605fd55b-fea7-474f-a0fe-a5e71af9b1ac
                Copyright © Copyright: © 2019 Journal of Conservative Dentistry
                License:

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                Date received : 06 June 2018
                Date revision received : 03 July 2018
                Date accepted : 02 September 2018
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Dentistry
                Keywords: nlrp1 and nlrc4,pulp,tooth
                Data availability:
                ScienceOpen disciplines: Dentistry
                Keywords: nlrp1 and nlrc4, pulp, tooth

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