Induction of TNF-α by Filifactor alocis in THP-1 macrophagic cells

被引：2

作者：

Kim, So-Hee ^{[1
]}

Kang, In-Chol ^{[1
,2
]}

机构：

[1] Chonnam Natl Univ, Sch Dent, Dept Oral Microbiol, Gwangju, South Korea

[2] 77,Yongbong ro, Gwangju, South Korea

来源：

ARCHIVES OF ORAL BIOLOGY | 2023年 / 155卷

关键词：

Filifactor alocis; Periodontal disease; THP-1; Tumor necrosis factor; Signaling pathway; ACTIVATION; INHIBITOR; AP-1;

D O I：

10.1016/j.archoralbio.2023.105806

中图分类号：

R78 [口腔科学];

学科分类号：

1003 ;

摘要：

Objectives: Filifactor alocis is an emerging periodontal pathogen, and macrophage-produced tumor necrosis factor-alpha (TNF-alpha) plays important roles in periodontal pathogenesis. In this study, we investigated F. alocis-stimulated TNF-alpha production in THP-1 macrophagic cells. Design: Phorbol 12-myristate 13-acetate-differentiated THP-1 macrophagic cells were challenged with F. alocis ATCC 35896 for various durations. TNF-alpha mRNA expression and protein secretion were determined using RT-PCR and ELISA, respectively. Activation of protein kinases and transcription factor proteins was evaluated by Western blot analysis. Results: Live F. alocis stimulated THP-1 cells to produce TNF-alpha in a dose-dependent manner. However, glutaraldehyde-killed or heat-killed F. alocis showed no effectiveness for TNF-alpha induction. In contrast, both live and killed Porphyromonas gingivalis robustly increased TNF-alpha expression. Furthermore, F. alocis was unable to stimulate TNF-alpha expression in Toll-like receptor 2 (TLR2) knockout THP-1 cells. F. alocis activated all three mitogen-activated protein kinases: extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK). Pharmacological inhibition of ERK and JNK, but not p38, significantly reduced F. alocis-induced TNF-alpha production. Finally, increased levels of phospho-c-Jun were detected in F. alocis-stimulated THP-1 cells. Conclusions: These results suggest that F. alocis induces TNF-alpha production in THP-1 macrophagic cells primarily by activating the TLR2, JNK, and c-Jun pathways.

引用

页数：5

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