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

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.

• Authors: Satoru Shindo, Yoshitaka Hosokawa, Ikuko Hosokawa, Hideki Shiba
• Journal: Inflammation (Inflammation) Vol. 42 Issue 3 Pg. 835-840 (Jun 2019) ISSN: 1573-2576 [Electronic] United States
• PMID: 30484005 (Publication Type: Journal Article)

Chemical References

• IL17A protein, human
• IL6 protein, human
• Interleukin-17
• Interleukin-6
• Interleukin-8
• Interleukins
• NF-kappa B
• interleukin-35, human
• Extracellular Signal-Regulated MAP Kinases

Topics

• Cells, Cultured
• Extracellular Signal-Regulated MAP Kinases (metabolism)
• Humans
• Interleukin-17 (pharmacology)
• Interleukin-6 (biosynthesis)
• Interleukin-8 (biosynthesis)
• Interleukins (pharmacology)
• NF-kappa B (metabolism)
• Periodontal Ligament (cytology, drug effects, metabolism)
• Periodontitis (prevention & control)
• Phosphorylation (drug effects)
• Signal Transduction (drug effects)
• T-Lymphocytes, Regulatory