Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende
Erweiterte Suche
Anmelden
nach oben
Inflammation
Erschienen in: Inflammation 3/2021

02.11.2020 | Original Article

The Effect of Porphyromonas gingivalis Lipopolysaccharide on the Pyroptosis of Gingival Fibroblasts

verfasst von: Yu-Yang Li, Qing Cai, Bao-Sheng Li, Shu-Wei Qiao, Jia-Yang Jiang, Dan Wang, Xue-Chun Du, Wei-Yan Meng

Erschienen in: Inflammation | Ausgabe 3/2021

Einloggen, um Zugang zu erhalten

Abstract

Periodontitis is a chronic inflammatory disease induced by Porphyromonas gingivalis (P. gingivalis) and other pathogens. P. gingivalis release various virulence factors including lipopolysaccharide (LPS). However, whether P. gingivalis–LPS inducing pyroptosis in human gingival fibroblasts (HGFs) remains unknown. In present study, P. gingivalis–LPS decreased the membrane integrity of HGFs, and pyroptosis-associated cytokines were upregulated at the mRNA level. In addition, pyroptosis proteins were highly expressed in gingival tissues of periodontitis. P. gingivalis–LPS induced gingivitis in the rat model, and the expression level of pyroptosis-associated proteins increased. Together, P. gingivalis–LPS can activate the pyroptosis reaction, which may be a pro-pyroptosis status in a relative low concentration.
Literatur
1.
Hiranmayi, K.V., K. Sirisha, M.V. Ramoji Rao, and P. Sudhakar. 2017. Novel pathogens in periodontal microbiology. Journal of Pharmacy & Bioallied Sciences 9 (3): 155–163.
2.
Genco, R.J. 1996. Current view of risk factors for periodontal diseases. Journal of Periodontology 67 (10s): 1041–1049.PubMed
3.
Dye, B.A. 2011. Global periodontal disease epidemiology. Periodontology 2000 58 (1): 10–25.
4.
Kolenbrander, P.E., R.N. Andersen, D.S. Blehert, P.G. Egland, J.S. Foster, and R.J. Palmer Jr. 2002. Communication among oral bacteria. Microbiology and Molecular Biology Reviews 66 (3): 486–505.PubMedPubMedCentral
5.
Silva, N., L. Abusleme, D. Bravo, N. Dutzan, J. Garcia-Sesnich, R. Vernal, et al. 2015. Host response mechanisms in periodontal diseases. Journal of Applied Oral Science 23 (3): 329–355.PubMedPubMedCentral
6.
Kroemer, G., P. Petit, N. Zamzami, J.L. Vayssière, and B. Mignotte. 1995. The biochemistry of programmed cell death. The FASEB Journal 9 (13): 1277–1287.PubMed
7.
8.
Sgorbissa, A., R. Benetti, S. Marzinotto, C. Schneider, and C. Brancolini. 1999. Caspase-3 and caspase-7 but not caspase-6 cleave Gas2 in vitro: implications for microfilament reorganization during apoptosis. Journal of Cell Science 112 (Pt 23): 4475–4482.PubMed
9.
Song, B., T. Zhou, W.L. Yang, J. Liu, and L.Q. Shao. 2017. Programmed cell death in periodontitis: recent advances and future perspectives. Oral Diseases 23 (5): 609–619.PubMed
10.
Nagata, S. 2018. Apoptosis and clearance of apoptotic cells. Annual Review of Immunology 36 (1): 489–517.PubMed
11.
Vanden Berghe, T., A. Linkermann, S. Jouan-Lanhouet, H. Walczak, and P. Vandenabeele. 2014. Regulated necrosis: the expanding network of non-apoptotic cell death pathways. Nature Reviews. Molecular Cell Biology 15 (2): 135–147.
12.
Someda, M., S. Kuroki, H. Miyachi, M. Tachibana, and S. Yonehara. 2020. Caspase-8, receptor-interacting protein kinase 1 (RIPK1), and RIPK3 regulate retinoic acid-induced cell differentiation and necroptosis. Cell Death and Differentiation 27 (5): 1539–1553.
13.
Li, J., X.J. Ke, F. Yan, L. Lei, and H. Li. 2018. Necroptosis in the periodontal homeostasis: signals emanating from dying cells. Oral Diseases 24 (6): 900–907.
14.
Ke, X., L. Lei, H. Li, H. Li, and F. Yan. 2016. Manipulation of necroptosis by porphyromonas gingivalis in periodontitis development. Molecular Immunology 77: 8–13.PubMed
15.
Awad, F., E. Assrawi, C. Louvrier, et al. 2018. Inflammasome biology, molecular pathology and therapeutic implications. Pharmacology & Therapeutics 187: 133–149.
16.
Brodsky, I.E., and D. Monack. 2009. NLR-mediated control of inflammasome assembly in the host response against bacterial pathogens. Seminars in Immunology 21 (4): 199–207.PubMed
17.
De Vasconcelos, N.M., N. Van Opdenbosch, H. Van Gorp, E. Parthoens, and M. Lamkanfi. 2019. Single-cell analysis of pyroptosis dynamics reveals conserved GSDMD-mediated subcellular events that precede plasma membrane rupture. Cell Death and Differentiation 26 (1): 146–161.
18.
Liu, X., Z. Zhang, J. Ruan, Y. Pan, V.G. Magupalli, H. Wu, and J. Lieberman. 2016. Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores. Nature 535 (7610): 153–158.PubMedPubMedCentral
19.
Yang, J., Y. Zhao, and F. Shao. 2015. Non-canonical activation of inflammatory caspases by cytosolic LPS in innate immunity. Current Opinion in Immunology 32: 78–83.PubMed
20.
Liu, J., J. Duan, Y. Wang, and X. Ouyang. 2014. Intracellular adhesion molecule-1 is regulated by Porphyromonas gingivalis through nucleotide binding oligomerization domain-containing proteins 1 and 2 molecules in periodontal fibroblasts. Journal of Periodontology 85 (2): 358–368.PubMed
21.
Liu, W., J. Liu, W. Wang, Y. Wang, and X. Ouyang. 2018. NLRP6 induces pyroptosis by activation of caspase-1 in gingival fibroblasts. Journal of Dental Research 97 (12): 1391–1398.PubMed
22.
Lamont, R.J., and H.F. Jenkinson. 1998. Life below the gum line: pathogenic mechanisms of Porphyromonas gingivalis. Microbiology and Molecular Biology Reviews 62 (4): 1244–1263.PubMedPubMedCentral
23.
Fitzsimmons, T.R., S. Ge, and P.M. Bartold. 2017. Compromised inflammatory cytokine response to P. gingivalis LPS by fibroblasts from inflamed human gingiva. Clinical Oral Investigations 22 (2): 919–927.PubMed
24.
Li, Y., J. Li, J. Sun, Y. Liu, D. Liu, L. Du, et al. 2020. Expression of RAD51 and its clinical impact in oral squamous cell carcinoma. Analytical Cellular Pathology 2020: 1827676.
25.
Li, Y., Z. Xu, J. Li, S. Ban, C. Duan, and W. Liu. 2018. Interleukin-18 expression in oral squamous cell carcinoma: its role in tumor cell migration and invasion, and growth of tumor cell xenografts. FEBS Open Bio 8 (12): 1953–1963.PubMedPubMedCentral
26.
Zenobia, C., and G. Hajishengallis. 2015. Porphyromonas gingivalis virulence factors involved in subversion of leukocytes and microbial dysbiosis. Virulence 6 (3): 236–243.PubMedPubMedCentral
27.
Makkawi, H., S. Hoch, E. Burns, K. Hosur, G. Hajishengallis, C.J. Kirschning, and G. Nussbaum. 2017. Porphyromonas gingivalis stimulates tlr2-pi3k signaling to escape immune clearance and induce bone resorption independently of myd88. Frontiers in Cellular and Infection Microbiology 7: 359.PubMedPubMedCentral
28.
Derradjia, A., H. Alanazi, H.J. Park, R. Djeribi, A. Semlali, and M. Rouabhia. 2015. α-Tocopherol decreases interleukin-1β and -6 and increases human β-defensin-1 and -2 secretion in human gingival fibroblasts stimulated with porphyromonas gingivalis lipopolysaccharide. Journal of Periodontal Research 51 (3): 295–303.PubMed
29.
Márton, I.J., and C. Kiss. 2014. Overlapping protective and destructive regulatory pathways in apical periodontitis. Journal of Endodontia 40 (2): 155–163.
30.
Novak, M.J., H.M. Albather, and J.M. Close. 2008. Redefining the biologic width in severe, generalized, chronic periodontitis: Implications for therapy. Journal of Periodontology 79 (10): 1864–1869.PubMed
31.
Graham-Engeland, J.E., N.L. Sin, J.M. Smyth, D.R. Jones, E.L. Knight, M.J. Sliwinski, and C.G. Engeland. 2018. Negative and positive affect as predictors of inflammation: timing matters. Brain, Behavior, and Immunity 74: 222–230.
32.
Hu, J., X. Liu, J. Zhao, et al. 2019. Identification of pyroptosis inhibitors that target a reactive cysteine in gasdermin D. Cancer Immunology Research 7 (2): A132.
33.
Shi, J., W. Gao, and F. Shao. 2017. Pyroptosis: gasdermin-mediated programmed necrotic cell death. Trends in Biochemical Sciences 42 (4): 245–254.PubMed
34.
Mulhall, H.J., A. Cardnell, K.F. Hoettges, F.H. Labeed, and M.P. Hughes. 2015. Apoptosis progression studied using parallel dielectrophoresis electrophysiological analysis and flow cytometry. Integrative Biology 7 (11): 1396–1401.PubMed
35.
Brentnall, M., L. Rodriguez-Menocal, R.L. De Guevara, E. Cepero, and L.H. Boise. 2013. Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis. BMC Cell Biology 14 (1): 32.PubMedPubMedCentral
36.
Xiang, H., F. Zhu, Z. Xu, and J. Xiong. 2020. Role of inflammasomes in kidney diseases via both canonical and non-canonical pathways. Frontiers in Cell and Development Biology 27 (8): 106.
37.
Vande, W.L., and M. Lamkanfi. 2016. Pyroptosis. Curr Biol, 2016 26 (13): R568–R572.
38.
Sborgi, L., S. Rühl, E. Mulvihill, J. Pipercevic, R. Heilig, H. Stahlberg, and S. Hiller. 2016. GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death. The EMBO Journal 35 (16): 1766–1778.PubMedPubMedCentral
39.
He, W.T., H. Wan, L. Hu, P. Chen, X. Wang, Z. Huang, Z.H. Yang, C.Q. Zhong, and J. Han. 2015. Gasdermin D is an executor of pyroptosis and required for interleukin-1β secretion. Cell Research 25 (12): 1285–1298.PubMedPubMedCentral
40.
Kayagaki, N., I.B. Stowe, B.L. Lee, K. O’Rourke, K. Anderson, S. Warming, T. Cuellar, B. Haley, M. Roose-Girma, Q.T. Phung, P.S. Liu, J.R. Lill, H. Li, J. Wu, S. Kummerfeld, J. Zhang, W.P. Lee, S.J. Snipas, G.S. Salvesen, L.X. Morris, L. Fitzgerald, Y. Zhang, E.M. Bertram, C.C. Goodnow, and V.M. Dixit. 2015. Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling. Nature 526 (7575): 666–671.PubMed
41.
Polito, L., M. Bortolotti, M. Pedrazzi, D. Mercatelli, M.G. Battelli, and A. Bolognesi. 2016. Apoptosis and necroptosis induced by stenodactylin in neuroblastoma cells can be completely prevented through caspase inhibition plus catalase or necrostatin-1. Phytomedicine 23 (1): 32–41.PubMed
42.
Fritsch, M., and Saskia D Günther, Schwarzer R, et al. 2019. Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis. Nature 575 (7784): 1–5.
43.
Chiquet, M., C. Katsaros, and D. Kletsas. 2015. Multiple functions of gingival and mucoperiosteal fibroblasts in oral wound healing and repair. Periodontology 2000 68 (1): 21–40.PubMed
44.
Tipton, D.A., A.A. Hatten, J.P. Babu, and MKh Dabbous. 2015. Effect of glycated albumin and cranberry components on interleukin-6 and matrix metalloproteinase-3 production by human gingival fibroblasts. Journal of Periodontal Research 51 (2): 228–236.PubMed
45.
Bozkurt, S.B., S.S. Hakki, E.E. Hakki, Y. Durak, and A. Kantarci. 2016. Porphyromonas gingivalis lipopolysaccharide induces a pro-inflammatory human gingival fibroblast phenotype. Inflammation 40 (1): 144–153.
46.
Jian-Yu, Gu, Yu-Jie Liu, Xiang-Qing Zhu, Jia-Ying Qiu, and Ying Sun. 2020. Effects of endotoxin tolerance induced by Porphyromonas gingivalis lipopolysaccharide on inflammatory responses in neutrophils. Inflammation 43 (5): 1692–1706.
47.
Jung, Y.J., H.K. Jun, and B.K. Choi. 2015. Contradictory roles of Porphyromonas gingivalis gingipains in caspase-1 activation. Cellular Microbiology 17 (9): 1304–1319.PubMed
48.
Fleetwood, A.J., M.K.S. Lee, W. Singleton, A. Achuthan, M.C. Lee, N.M. O'Brien-Simpson, et al. 2017. Metabolic remodeling, Inflammasome activation, and pyroptosis in macrophages stimulated by Porphyromonas gingivalis and its outer membrane vesicles. Frontiers in Cellular and Infection Microbiology 4 (7): 351.
49.
Cheng, R., W. Liu, R. Zhang, Y. Feng, N.A. Bhowmick, and T. Hu. 2017. Porphyromonas gingivalis-derived lipopolysaccharide combines hypoxia to induce caspase-1 activation in periodontitis. Frontiers in Cellular and Infection Microbiology 14 (7): 474.
50.
Li, Y.Y., B.S. Li, W.W. Liu, Q. Cai, H.Y. Wang, Y.Q. Liu, Y.J. Liu, and W.Y. Meng. 2020. Effects of D-arginine on Porphyromonas gingivalis biofilm. Journal of Oral Science 62 (1): 57–61.PubMed
Metadaten
Titel
The Effect of Porphyromonas gingivalis Lipopolysaccharide on the Pyroptosis of Gingival Fibroblasts
verfasst von
Yu-Yang Li
Qing Cai
Bao-Sheng Li
Shu-Wei Qiao
Jia-Yang Jiang
Dan Wang
Xue-Chun Du
Wei-Yan Meng
Publikationsdatum
02.11.2020
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 3/2021
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-020-01379-7

Weitere Artikel der Ausgabe 3/2021

Inflammation 3/2021 Zur Ausgabe

Original Article

Tadalafil Alleviates LPS-Induced Inflammation and Oxidative Stress of RWPE-1 Cell by Regulating the Akt/Nrf2 Signaling Pathway

Correction

Correction to: Inhibition of C3a/C3aR Axis in Diverse Stages of Ulcerative Colitis Affected the Prognosis of UC by Modulating the Pyroptosis and Expression of Caspase-11

Original Article

The Anti-inflammatory Protein TSG-6 Induced by S. aureus Regulates the Chemokine Function of Endothelial Cells In Vitro by Inhibiting the Chemokine-Glycosaminoglycan Interaction

Original Article

Amelioration of Juglanin against LPS-Induced Activation of NLRP3 Inflammasome in Chondrocytes Mediated by SIRT1

Original Article

Hydroxysafflor Yellow A Inhibits Staphylococcus aureus-Induced Mouse Endometrial Inflammation via TLR2-Mediated NF-kB and MAPK Pathway

Original Article

Progesterone Attenuates Brain Inflammatory Response and Inflammation-Induced Increase in Immature Myeloid Cells in a Mouse Model

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

Reizdarmsyndrom: Diäten wirksamer als Medikamente

29.04.2024 Reizdarmsyndrom Nachrichten

Bei Reizdarmsyndrom scheinen Diäten, wie etwa die FODMAP-arme oder die kohlenhydratreduzierte Ernährung, effektiver als eine medikamentöse Therapie zu sein. Das hat eine Studie aus Schweden ergeben, die die drei Therapieoptionen im direkten Vergleich analysierte.

Notfall-TEP der Hüfte ist auch bei 90-Jährigen machbar

26.04.2024 Hüft-TEP Nachrichten

Ob bei einer Notfalloperation nach Schenkelhalsfraktur eine Hemiarthroplastik oder eine totale Endoprothese (TEP) eingebaut wird, sollte nicht allein vom Alter der Patientinnen und Patienten abhängen. Auch über 90-Jährige können von der TEP profitieren.

Niedriger diastolischer Blutdruck erhöht Risiko für schwere kardiovaskuläre Komplikationen

25.04.2024 Hypotonie Nachrichten

Wenn unter einer medikamentösen Hochdrucktherapie der diastolische Blutdruck in den Keller geht, steigt das Risiko für schwere kardiovaskuläre Ereignisse: Darauf deutet eine Sekundäranalyse der SPRINT-Studie hin.

Bei schweren Reaktionen auf Insektenstiche empfiehlt sich eine spezifische Immuntherapie

25.04.2024 Allergien und Intoleranzreaktionen Nachrichten

Insektenstiche sind bei Erwachsenen die häufigsten Auslöser einer Anaphylaxie. Einen wirksamen Schutz vor schweren anaphylaktischen Reaktionen bietet die allergenspezifische Immuntherapie. Jedoch kommt sie noch viel zu selten zum Einsatz.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen
Bildnachweise