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 3/2019

27.11.2018 | ORIGINAL ARTICLE

Interleukin (IL)-35 Suppresses IL-6 and IL-8 Production in IL-17A-Stimulated Human Periodontal Ligament Cells

verfasst von: Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Hideki Shiba

Erschienen in: Inflammation | Ausgabe 3/2019

Einloggen, um Zugang zu erhalten

Abstract

Interleukin (IL)-35 is a novel anti-inflammatory cytokine that is produced by regulatory T cells. IL-35 is reported to suppress IL-17A-producing helper T (Th17) cell activation. IL-17A is related to progression of periodontitis. Furthermore, IL-35 and IL-17A are detected in human gingival crevicular fluid. However, the effect of IL-35 and interaction between IL-35 and IL-17A on pro-inflammatory cytokine production in human periodontal resident cells are still unclear. The aim of this study was to clarify the effect of IL-35 on IL-6 and IL-8 production in human periodontal ligament cells (HPDLCs) stimulated with IL-17A. IL-35 inhibited IL-6 and IL-8 production in IL-17A-stimulated HPDLCs. Moreover, western blot analysis showed that IL-35 suppressed extracellular signal-regulated kinase (ERK) and nuclear factor (NF)-κB p65 phosphorylation in IL-17A-stimulated HPDLCs. Our findings suggested that IL-35 produced from regulatory T cells might inhibit progression of periodontitis by decreasing IL-17A-induced levels of IL-6 and IL-8.
Literatur
1.
Taubman, M.A., H. Yoshie, J.L. Ebersole, D.J. Smith, and C.L. Olson. 1984. Host response in experimental periodontal disease. Journal of Dental Research 63: 455–460.CrossRef
2.
Cardoso, C.R., G.P. Garlet, G.E. Crippa, A.L. Rosa, W.M. Júnior, M.A. Rossi, and J.S. Silva. 2009. Evidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease. Oral Microbiology and Immunology 24: 1–6.CrossRef
3.
Kotake, S., N. Udagawa, N. Takahashi, K. Matsuzaki, K. Itoh, S. Ishiyama, S. Saito, K. Inoue, N. Kamatani, M.T. Gillespie, T.J. Martin, and T. Suda. 1999. IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. Journal of Clinical Investigation 103: 1345–1352.CrossRef
4.
Shibata, M., Y. Shintaku, K. Matsuzaki, and S. Uematsu. 2014. The effect of IL-17 on the production of proinflammatory cytokines and matrix metalloproteinase-1 by human periodontal ligament fibroblasts. Orthodontics & Craniofacial Research 17 (1): 60–68.CrossRef
5.
Bendtzen, K. 1988. Interleukin 1, interleukin 6 and tumor necrosis factor in infection, inflammation and immunity. Immunology Letters 19: 183–191.CrossRef
6.
Hashizume, M., N. Hayakawa, and M. Mihara. 2008. IL-6 trans-signalling directly induces RANKL on fibroblast-like synovial cells and is involved in RANKL induction by TNF-alpha and IL-17. Rheumatology 47: 1635–1640.CrossRef
7.
Bettelli, E., Y. Carrier, W. Gao, T. Korn, T.B. Strom, M. Oukka, H.L. Weiner, and V.K. Kuchroo. 2006. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 441: 235–238.CrossRef
8.
Fredriksson, M., K. Bergström, and B. Asman. 2002. IL-8 and TNF-alpha from peripheral neutrophils and acute-phase proteins in periodontitis. Journal of Clinical Periodontology 29: 123–128.CrossRef
9.
Devergne, O., M. Birkenbach, and E. Kieff. 1997. Epstein–Barr virus-induced gene 3 and the p35 subunit of interleukin 12 form a novel heterodimeric hematopoietin. Proceedings of the National Academy of Sciences 94: 12041–12046.CrossRef
10.
Collison, L.W., C.J. Workman, T.T. Kuo, K. Boyd, Y. Wang, K.M. Vignali, R. Cross, D. Sehy, R.S. Blumberg, and D.A. Vignali. 2007. The inhibitory cytokine IL-35 contributes to regulatory T-cell function. Nature 450: 566–569.CrossRef
11.
Shen, P., T. Roch, V. Lampropoulou, R.A. O'Connor, U. Stervbo, E. Hilgenberg, S. Ries, V.D. Dang, Y. Jaimes, C. Daridon, R. Li, L. Jouneau, P. Boudinot, S. Wilantri, I. Sakwa, Y. Miyazaki, M.D. Leech, R.C. McPherson, S. Wirtz, M. Neurath, K. Hoehlig, E. Meinl, A. Grützkau, J.R. Grün, K. Horn, A.A. Kühl, T. Dörner, A. Bar-Or, S.H.E. Kaufmann, S.M. Anderton, and S. Fillatreau. 2014. IL-35-producing B cells are critical regulators of immunity during autoimmune and infectious diseases. Nature 507: 366–370.CrossRef
12.
Olson, B.M., E. Jankowska-Gan, J.T. Becker, D.A. Vignali, W.J. Burlingham, and D.G. McNeel. 2012. Human prostate tumor antigen-specific CD8+ regulatory T cells are inhibited by CTLA-4 or IL-35 blockade. Journal of Immunology 189: 5590–5601.CrossRef
13.
Okada, K., T. Fujimura, T. Kikuchi, M. Aino, Y. Kamiya, A. Izawa, Y. Iwamura, H. Goto, I. Okabe, E. Miyake, Y. Hasegawa, M. Mogi, and A. Mitani. 2017. Effect of interleukin (IL)-35 on IL-17 expression and production by human CD4+ T cells. PeerJ 5: e2999.CrossRef
14.
Wang, R.X., C.R. Yu, R.M. Mahdi, and C.E. Egwuagu. 2012. Novel IL27p28/IL12p40 cytokine suppressed experimental autoimmune uveitis by inhibiting autoreactive Th1/Th17 cells and promoting expansion of regulatory T cells. Journal of Biological Chemistry 287: 36012–36021.CrossRef
15.
Thiolat, A., A. Denys, M. Petit, J. Biton, D. Lemeiter, R. Herve, D. Lutomski, M.C. Boissier, and N. Bessis. 2014. Interleukin-35 gene therapy exacerbates experimental rheumatoid arthritis in mice. Cytokine 69: 87–93.CrossRef
16.
Mitani, A., W. Niedbala, T. Fujimura, M. Mogi, S. Miyamae, N. Higuchi, A. Abe, T. Hishikawa, M. Mizutani, Y. Ishihara, H. Nakamura, K. Kurita, N. Ohno, Y. Tanaka, M. Hattori, and T. Noguchi. 2015. Increased expression of interleukin (IL)-35 and IL-17, but not IL-27, in gingival tissues with chronic periodontitis. Journal of Periodontology 86: 301–309.CrossRef
17.
Shindo, S., Y. Hosokawa, I. Hosokawa, K. Ozaki, and T. Matsuo. 2014. Genipin inhibits IL-1β-induced CCL20 and IL-6 production from human periodontal ligament cells. Cellular Physiology and Biochemistry 33: 357–364.CrossRef
18.
Jung, Y.J., Y.J. Choi, S.J. An, H.R. Lee, H.K. Jun, and B.K. Choi. 2017. Tannerella forsythia GroEL induces inflammatory bone resorption and synergizes with interleukin-17. Molecular Oral Microbiology 32: 301–313.CrossRef
19.
Köseoğlu, S., M. Sağlam, T. Pekbağrıyanık, L. Savran, and R. Sütçü. 2015. Level of interleukin-35 in gingival crevicular fluid, saliva, and plasma in periodontal disease and health. Journal of Periodontology 24: 1–6.
20.
Wilson, N.J., K. Boniface, J.R. Chan, B.S. McKenzie, W.M. Blumenschein, J.D. Mattson, B. Basham, K. Smith, T. Chen, F. Morel, J.C. Lecron, R.A. Kastelein, D.J. Cua, T.K. McClanahan, E.P. Bowman, and Malefyt R. de Waal. 2007. Development, cytokine profile and function of human interleukin 17-producing helper T cells. Nature Immunology 8: 950–957.CrossRef
21.
Takahashi, K., T. Azuma, H. Motohira, D.F. Kinane, and S. Kitetsu. 2005. The potential role of interleukin-17 in the immunopathology of periodontal disease. Journal of Clinical Periodontology 32: 369–374.CrossRef
22.
Lin, D., L. Li, Y. Sun, W. Wang, X. Wang, Y. Ye, X. Chen, and Y. Xu. 2014. IL-17 regulates the expressions of RANKL and OPG in human periodontal ligament cells via TRAF6/TBK1-JNK/NF-κB pathways. Immunology 144: 472–485.CrossRef
23.
Wu, Y., L. Zhu, L. Liu, J. Zhang, and B. Peng. 2014. Interleukin-17A stimulates migration of periodontal ligament fibroblasts via p38 MAPK/NF-κB-dependent MMP-1 expression. Journal of Cellular Physiology 229: 292–299.CrossRef
24.
Wang, Y., Y. Mao, J. Zhang, G. Shi, L. Cheng, Y. Lin, Y. Li, X. Zhang, Y. Zhang, X. Chen, J. Deng, X. Su, L. Dai, Y. Yang, S. Zhang, D. Yu, Y. Wei, and H. Deng. 2018. IL-35 recombinant protein reverses inflammatory bowel disease and psoriasis through regulation of inflammatory cytokines and immune cells. Journal of Cellular and Molecular Medicine 22: 1014–1025.PubMed
25.
Zhang, X.H., Y. Zhou, J.M. Zhang, S.Y. Zhou, M. Wang, R. Feng, F.E. Feng, Q.M. Wang, X.L. Zhu, X.S. Zhao, M. Lv, Y. Kong, Y.J. Chang, and X.J. Huang. 2015. IL-35 inhibits acute graft-versus-host disease in a mouse model. International Immunopharmacology 29: 383–392.CrossRef
26.
Wu, S., Y. Li, Y. Li, L. Yao, T. Lin, S. Jiang, H. Shen, L. Xia, and J. Lu. 2016. Interleukin-35 attenuates collagen-induced arthritis through suppression of vascular endothelial growth factor and its receptors. International Immunopharmacology 34: 71–77.CrossRef
27.
Hu, L., C. Chen, J. Zhang, K. Wu, X. Zhang, H. Liu, and J. Hou. 2017. IL-35 pretreatment alleviates lipopolysaccharide-induced acute kidney injury in mice by inhibiting NF-κB activation. Inflammation 40: 1393–1400.CrossRef
28.
Chen, X., S. Hao, Z. Zhao, J. Liu, Q. Shao, F. Wang, D. Sun, Y. He, W. Gao, and H. Mao. 2018. Interleukin 35: inhibitory regulator in monocyte-derived dendritic cell maturation and activation. Cytokine 108: 43–52.CrossRef
29.
Sha, X., S. Meng, X. Li, H. Xi, M. Maddaloni, D.W. Pascual, H. Shan, X. Jiang, H. Wang, and X.F. Yang. 2015. Interleukin-35 inhibits endothelial cell activation by suppressing MAPK-AP-1 pathway. Journal of Biological Chemistry 290: 19307–19318.CrossRef
Metadaten
Titel
Interleukin (IL)-35 Suppresses IL-6 and IL-8 Production in IL-17A-Stimulated Human Periodontal Ligament Cells
verfasst von
Satoru Shindo
Yoshitaka Hosokawa
Ikuko Hosokawa
Hideki Shiba
Publikationsdatum
27.11.2018
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 3/2019
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-018-0938-9

Weitere Artikel der Ausgabe 3/2019

Inflammation 3/2019 Zur Ausgabe

ORIGINAL ARTICLE

Aging and Hyperglycemia Intensify Dyslipidemia-Induced Oxidative Stress and Inflammation in Rats: Assessment of Restorative Potentials of ALA and EPA + DHA

ORIGINAL ARTICLE

Inhibition of Carrageenan/Kaolin-Induced Arthritis in Rats and of Inflammatory Cytokine Expressions in Human IL-1β-Stimulated Fibroblast-like Synoviocytes by a Benzylideneacetophenone Derivative

ORIGINAL ARTICLE

Baicalein Inhibits the IL-1β-Induced Inflammatory Response in Nucleus Pulposus Cells and Attenuates Disc Degeneration In vivo

ORIGINAL ARTICLE

Short-Term Effects of Sepsis and the Impact of Aging on the Transcriptional Profile of Different Brain Regions

ORIGINAL ARTICLE

Saroglitazar Deactivates the Hepatic LPS/TLR4 Signaling Pathway and Ameliorates Adipocyte Dysfunction in Rats with High-Fat Emulsion/LPS Model-Induced Non-alcoholic Steatohepatitis

ORIGINAL ARTICLE

Periodontal Injection of Lipopolysaccharide Promotes Arthritis Development in Mice

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

Erhöhte Mortalität bei postpartalem Brustkrebs

07.05.2024 Mammakarzinom Nachrichten

Auch für Trägerinnen von BRCA-Varianten gilt: Erkranken sie fünf bis zehn Jahre nach der letzten Schwangerschaft an Brustkrebs, ist das Sterberisiko besonders hoch.

Hypertherme Chemotherapie bietet Chance auf Blasenerhalt

07.05.2024 Harnblasenkarzinom Nachrichten

Eine hypertherme intravesikale Chemotherapie mit Mitomycin kann für Patienten mit hochriskantem nicht muskelinvasivem Blasenkrebs eine Alternative zur radikalen Zystektomie darstellen. Kölner Urologen berichten über ihre Erfahrungen.

Ein Drittel der jungen Ärztinnen und Ärzte erwägt abzuwandern

07.05.2024 Medizinstudium Nachrichten

Extreme Arbeitsverdichtung und kaum Supervision: Dr. Andrea Martini, Sprecherin des Bündnisses Junge Ärztinnen und Ärzte (BJÄ) über den Frust des ärztlichen Nachwuchses und die Vorteile des Rucksack-Modells.

Vorhofflimmern bei Jüngeren gefährlicher als gedacht

06.05.2024 Vorhofflimmern Nachrichten

Immer mehr jüngere Menschen leiden unter Vorhofflimmern. Betroffene unter 65 Jahren haben viele Risikofaktoren und ein signifikant erhöhtes Sterberisiko verglichen mit Gleichaltrigen ohne die Erkrankung.

Update Innere Medizin

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

Newsletter bestellen
Bildnachweise