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      SPRC Suppresses Experimental Periodontitis by Modulating Th17/Treg Imbalance

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          Abstract

          Object: The aims of the study were to explore the protective effects of S-propargyl-cysteine (SPRC) on periodontitis and to determine the underlying mechanisms.

          Methods: A rat periodontitis model was constructed by injecting LPS and SPRC (0, 25, and 50 mg/kg/d) was administered intraperitoneally. H2S and CSE level were detected. The alveolar bone level was evaluated by micro-CT, HE staining and methylene blue staining analysis. Inflammation-related factors, Treg and Th17 cells were detected by immunohistochemistry, RT-PCR, immunofluorescence, Western blot and flow cytometry. Phosphorylation levels of ERK1/2 and CREB were analysed.

          Results: The administration of SPRC significantly increased the expression of CSE in the gingival tissue and the concentration of endogenous H2S in the peripheral blood. Simultaneously, SPRC significantly inhibited the resorption of alveolar bone based on the H&E staining, micro-CT and methylene blue staining analysis. Compared with the periodontitis group, the levels of IL-17A, IL-10 were downregulated and IL-6,TGF-β1 were upregulated in the SPRC groups. In the SPRC group, the percentage of TH17 cells and the expression of ROR-γt were downregulated, while the percentage of Tregs and the expression of Foxp3 were upregulated accompanied with inhibition of phosphorylation ERK1/2 and CREB.

          Conclusion: SPRC can prevent the progression of periodontitis by regulating the Th17/Treg balance by inhibition of the ERK/CREB signalling pathway.

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          Periodontitis: from microbial immune subversion to systemic inflammation.

          George Hajishengallis (2015)
          Periodontitis is a dysbiotic inflammatory disease with an adverse impact on systemic health. Recent studies have provided insights into the emergence and persistence of dysbiotic oral microbial communities that can mediate inflammatory pathology at local as well as distant sites. This Review discusses the mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extra-oral sites.
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            Inflammatory and immune pathways in the pathogenesis of periodontal disease.

            Ali CEKICI, Alpdogan Kantarci, Hatice Hasturk … (2014)
            The pathogenesis of periodontitis involves a complex immune/inflammatory cascade that is initiated by the bacteria of the oral biofilm that forms naturally on the teeth. The susceptibility to periodontitis appears to be determined by the host response; specifically, the magnitude of the inflammatory response and the differential activation of immune pathways. The purpose of this review was to delineate our current knowledge of the host response in periodontitis. The role of innate immunity, the failure of acute inflammation to resolve (thus becoming chronic), the cytokine pathways that regulate the activation of acquired immunity and the cells and products of the immune system are considered. New information relating to regulation of both inflammation and the immune response will be reviewed in the context of susceptibility to, and perhaps control of, periodontitis. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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              The Balance of Th17 versus Treg Cells in Autoimmunity

              Gap Ryol Lee (2018)
              T helper type 17 (Th17) cells and pTreg cells, which share a common precursor cell (the naïve CD4 T cell), require a common tumor growth factor (TGF)-β signal for initial differentiation. However, terminally differentiated cells fulfill opposite functions: Th17 cells cause autoimmunity and inflammation, whereas Treg cells inhibit these phenomena and maintain immune homeostasis. Thus, unraveling the mechanisms that affect the Th17/Treg cell balance is critical if we are to better understand autoimmunity and tolerance. Recent studies have identified many factors that influence this balance; these factors range from signaling pathways triggered by T cell receptors, costimulatory receptors, and cytokines, to various metabolic pathways and the intestinal microbiota. This review article summarizes recent advances in our understanding of the Th17/Treg balance and its implications with respect to autoimmune disease.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Bioeng Biotechnol
                Journal ID (iso-abbrev): Front Bioeng Biotechnol
                Journal ID (publisher-id): Front. Bioeng. Biotechnol.
                Title: Frontiers in Bioengineering and Biotechnology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 2296-4185
                Publication date (Electronic): 11 January 2022
                Publication date Collection: 2021
                Volume: 9
                Electronic Location Identifier: 737334
                Affiliations
                [1] 1 Department of Stomatology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine , Shanghai, China
                [2] 2 Hubei No. 3 People’s Hospital of Jianghan University , Wuhan, China
                [3] 3 Pharmacy Department, Minda Hospital of Hubei Minzu University , Enshi, China
                [4] 4 Medical College of Anhui University of Science and Technology , Huainan, China
                [5] 5 Jiading Central Hospital, Shanghai University of Medicine and Health Sciences , Shanghai, China
                [6] 6 The First People’s Hospital of KunShan , Kunshan, China
                [7] 7 State Key Laboratory of Quality Research in Chinese Medicine and School of Pharmacy, Macau University of Science and Technology , Taipa, Macao SAR, China
                [8] 8 Department of Prothodontics, Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital, Fudan University , Shanghai, China
                Author notes

                Edited by: Bryan Brown, University of Pittsburgh, United States

                Reviewed by: Xiaoping Lin, ShengJing Hospital of China Medical University, China

                Karina Nakayama, Oregon Health and Science University, United States

                *Correspondence: Yizhun Zhu, yzzhu@ 123456must.edu.mo ; Raorao Wang, raoraowang@ 123456hotmail.com ; Shengcai Qi, dentistqi@ 123456163.com
                [ † ]

                These authors have contributed equally to this work

                This article was submitted to Tissue Engineering and Regenerative Medicine, a section of the journal Frontiers in Bioengineering and Biotechnology

                Article
                Publisher ID: 737334
                DOI: 10.3389/fbioe.2021.737334
                PMC ID: 8787365
                PubMed ID: 35087796
                SO-VID: c484c298-b8d3-4570-8c87-49bd6a0464a6
                Copyright © Copyright © 2022 Peng, Zhao, Lin, Liu, Zhou, Lan, Yao, Cong, Tao, Zhu, Wang and Qi.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 06 July 2021
                Date accepted : 16 December 2021
                Funding
                Funded by: Natural Science Foundation of Shanghai , doi 10.13039/100007219;
                Categories
                Subject: Bioengineering and Biotechnology
                Subject: Original Research

                Keywords: s-propargyl-cysteine,periodontitis,th17 cells,regulatory t cells,erk/creb signalling pathway
                Data availability:
                Keywords: s-propargyl-cysteine, periodontitis, th17 cells, regulatory t cells, erk/creb signalling pathway

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