Innate immune response of human periodontal ligament fibroblasts via the Dectin-1/Syk pathway

锡克 酵母多糖 白色念珠菌 先天免疫系统 免疫系统 生物 微生物学 污渍 流式细胞术 白色体 免疫学 细胞生物学 信号转导 生物化学 基因 体外 酪氨酸激酶
作者
Megumi Inomata,Shigeru Amano,MASAYO ABE,Toru Hayashi,Hiroshi Sakagami
出处
期刊:Journal of Medical Microbiology [Microbiology Society]
卷期号:71 (12) 被引量:5
标识
DOI:10.1099/jmm.0.001627
摘要

Introduction. A diverse microbiota including fungi exists in the subgingival sites of patients with chronic periodontitis. The cell wall of Candida albicans, the most abundant fungal species, contains β-glucan. Dectin-1 binds β-glucan and participates in fungal recognition.Gap statement. Human periodontal ligament fibroblasts (PDLFs) are present in the periodontal ligament and synthesize immunomodulatory cytokines that influence the local response to infections. However, the expression and role of Dectin-1 in PDLFs have not been explored.Aim. This study aimed to determine if PDLFs express Dectin-1 and induce innate immune responses through Dectin-1 and the signalling molecule Syk.Methodology. The expression of Dectin-1 in PDLFs was determined by flow cytometry, western blotting and confocal microscopy. Real-time PCR and Western blotting were used to determine the immune response of PDLFs stimulated with β-glucan-rich zymosan and C. albicans.Results. Dectin-1 was constitutively expressed in PDLFs. Zymosan induced the expression of cytokines, including IL6, IL1B and IL17A, and the chemokine IL8. Zymosan also induced the expression of the antimicrobial peptide β-defensin-1 (DEFB1). Further, the phosphorylation of Syk and NF-κB occurred upon Dectin-1 activation. Notably, heat-killed C. albicans induced the expression of IL6, IL17A, IL8 and DEFB1, and this activation was suppressed by the Syk inhibitor, R406.Conclusion. These findings indicate that the Dectin-1/Syk pathway induces an innate immune response of PDLFs, which may facilitate the control of oral infections such as candidiasis and periodontitis.

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