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Lipopolysaccharide (LPS) of Porphyromonas gingivalis induces IL-1β, TNF- and IL-6 production by THP-1 cells in a way different from that of Escherichia coli LPS

Department of Stomatology, The Second Afiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China

Lili Chen

Department of Stomatology, The Second Afiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China, yanchen_5657{at}163.com

Shenglai Li

Department of Oral and Maxillofacial Surgery, Stomatology Hospital, School of Medicine, Zhejiang University, Hangzhou, China

Zhiyuan Gu

Department of Oral and Maxillofacial Surgery, Stomatology Hospital, School of Medicine, Zhejiang University, Hangzhou, China

Jie Yan

Department of Microbiology and Parasitology, School of Medicine, Zhejiang University, Hangzhou, China, med_bp{at}zju.edu.cn

Lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis has been shown to differ from enterobacterial LPS in structure and function; therefore, the Toll-like receptors (TLRs) and the intracellular inflammatory signaling pathways are accordingly different. To elucidate the signal transduction pathway of P. gingivalis, LPS-induced pro-inflammatory cytokine production in the human monocytic cell line THP-1 was measured by ELISA, and the TLRs were determined by the blocking test using anti-TLRs antibodies. In addition, specific inhibitors as well as Phospho-ELISA kits were used to analyze the intracellular signaling pathways. Escherichia coli LPS was used as the control. In this study, P. gingivalis LPS showed the ability to induce cytokine production in THP-1 cells and its induction was significantly (P < 0.05) suppressed by anti-TLR2 antibody or JNK inhibitor, and the phosphorylation level of JNK was significantly increased (P < 0.05). These results indicate that TLR2—JNK is the main signaling pathway of P. gingivalis LPS-induced cytokine production, while the cytokine induction by E. coli LPS was mainly via TLR4—NF-B and TLR4—p38MAPK. This suggests that P. gingivalis LPS differs from E. coli LPS in its signaling pathway in THP-1 cells, and that the TLR2—JNK pathway might play a significant role in P. gingivalis LPS-induced chronic inflammatory periodontal disease.

Key Words: Lipopolysaccharide • Porphyromonas gingivalis • signaling pathway • THP-1 cells • cytokines

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