Increase of CCL20 expression by human gingival fibroblasts upon stimulation with cytokines and bacterial endotoxin

• Published in: Clinical and experimental immunology Vol. 142; no. 2; pp. 285 - 291
• Main Authors: Hosokawa, Y., Hosokawa, I., Ozaki, K., Nakae, H., Matsuo, T.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.11.2005; Blackwell; Oxford University Press; Blackwell Science Inc
• Subjects: Adult; Basic Immunology; Biological and medical sciences; CCL20; Cells, Cultured; Chemokine CCL20; Chemokines, CC - biosynthesis; Chemokines, CC - genetics; Cytokines - immunology; Enzyme Inhibitors - pharmacology; Escherichia coli; Extracellular Signal-Regulated MAP Kinases - immunology; Female; fibroblast; Fibroblasts - immunology; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Gene Expression Regulation - immunology; Gingiva - immunology; Humans; Immunopathology; Interferon-gamma - immunology; Interleukin-1 - immunology; JNK Mitogen-Activated Protein Kinases - immunology; Lipopolysaccharides - immunology; Macrophage Inflammatory Proteins - biosynthesis; Macrophage Inflammatory Proteins - genetics; Medical sciences; NF-kappa B - immunology; p38 Mitogen-Activated Protein Kinases - immunology; periodontal disease; Reverse Transcriptase Polymerase Chain Reaction - methods; RNA, Messenger - genetics; Signal Transduction - immunology; Tumor Necrosis Factor-alpha - immunology; Vascular Endothelial Growth Factor A - biosynthesis; Human; Immunopathology; Stomatology; CCL20; Cytokine; Stimulation; Dentistry; Endotoxin; Toxin; Periodontal disease; Immunology; Bacteria; Periodontopathy; Fibroblast
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.2005.02912.x

Summary We have demonstrated recently that CCL20 was expressed in periodontal diseased tissues and abundant CCR6 positive T cells infiltrated in periodontally diseased tissue. However, it is uncertain which cells can elicit CCL20 production. In the present study, we examined the properties of CCL20 production by human gingival fibroblasts (HGF) culture. Here, we report that interleukin‐1 beta (IL‐1β), tumour necrosis factor‐alpha (TNF‐α) and Escherichia coli lipopolysaccharide (LPS) can significantly induce the production of CCL20 by HGF. We found that TNF‐α and E. coli LPS enhanced the production of CCL20 by HGF treated with IL‐1β. In contrast, interferon‐gamma (IFN‐γ) dramatically diminished CCL20 production induced by IL‐1β. Moreover, we demonstrated that nuclear factor‐kappaB (NF‐κB), p38 mitogen‐activated protein kinase (MAPK) and extracellular signal‐regulated kinases (ERK) play an important role in mediating the production of CCL20 induced by IL‐1β and TNF‐α. On the other hand, we found that not only NF‐κB, p38 MAPK and ERK but also c‐Jun NH2‐terminal kinase (JNK) are involved in CCL20 production induced by E. coli LPS. Finally, we found that HGF express CCR6, CCL20 receptor, and CCL20 induced vascular endothelial growth factor (VEGF) by HGF. Taken together, these findings that HGF will be a source of CCL20 in periodontal tissue, and the CCL20 production will be controlled by proinflammatory cytokine and bacterial LPS in periodontally diseased tissue. Thus, CCL20 by HGF might be involved in inflammatory cells infiltration, and promote the progression of periodontal disease.