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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells
Published on: December 17, 2015
Mechanisms of Porphyromonas gingivalis-induced monocyte chemoattractant protein-1 expression in endothelial cells
Eun-Kyoung Choi1, Sun-Ah Park, Won-Mann Oh
1Department of Oral Microbiology, Chonnam National University Dental School, 300 Yongbong-Dong, Puk-Gu, Kwangju 500-757, South Korea.
Abstract:
Monocyte chemoattractant protein-1 (MCP-1) is expressed in vascular endothelial cells of inflamed gingival tissues and plays an important role in periodontal pathogenesis. Endothelial cells produce high levels of MCP-1 in response to Porphyromonas gingivalis, an important periodontal pathogen. The present study investigated the mechanisms involved in MCP-1 production by human umbilical vein endothelial cells (HUVEC) following infection with P. gingivalis. In contrast to P. gingivalis, Bacteroides forsythus only weakly stimulated MCP-1 production while Treponema denticola could not induce MCP-1 in HUVEC. The MCP-1 production was independent of endogenous interleukin (IL)-1alpha as IL-1 receptor antagonist treatment did not reduce MCP-1 production by P. gingivalis. Meanwhile, antioxidant treatment and inhibition of NAD(P)H oxidase significantly reduced MCP-1 production. Pharmacological inhibition of p38 mitogen-associated protein (MAP) kinase, c-Jun N-terminal kinase (JNK), nuclear factor-kappaB (NF-kappaB) or activator protein-1 (AP-1) also substantially attenuated P. gingivalis-induced MCP-1 expression by HUVEC. Indeed, activation of NF-kappaB and AP-1 was observed in P. gingivalis-infected HUVEC. These results suggest that MCP-1 expression is upregulated in P. gingivalis-infected endothelial cells via reactive oxygen species, p38 MAP kinase, JNK, NF-kappaB, and AP-1.
Insights
Porphyromonas gingivalis infection upregulates monocyte chemoattractant protein-1 (MCP-1) in endothelial cells. This process involves reactive oxygen species and signaling pathways including p38 MAP kinase, JNK, NF-kappaB, and AP-1.
Area of Science:
- Periodontal pathogenesis
- Endothelial cell biology
- Infectious disease mechanisms
Background:
- Monocyte chemoattractant protein-1 (MCP-1) is crucial in inflamed gingival tissues and periodontal pathogenesis.
- Endothelial cells significantly increase MCP-1 production when exposed to Porphyromonas gingivalis, a key periodontal pathogen.
Purpose of the Study:
- To elucidate the molecular mechanisms driving MCP-1 production in human umbilical vein endothelial cells (HUVEC) after P. gingivalis infection.
- To differentiate the effects of P. gingivalis from other periodontal bacteria like Bacteroides forsythus and Treponema denticola on MCP-1 production.
Main Methods:
- Assessing MCP-1 production in HUVEC stimulated with different periodontal pathogens.
- Investigating the role of interleukin (IL)-1alpha by using IL-1 receptor antagonist.
- Evaluating the impact of antioxidant treatment and NAD(P)H oxidase inhibition on MCP-1 levels.
- Examining the effects of inhibiting specific signaling pathways: p38 MAP kinase, JNK, NF-kappaB, and AP-1.
Main Results:
- P. gingivalis strongly induced MCP-1 production in HUVEC, while B. forsythus had a weak effect and T. denticola had no effect.
- MCP-1 production was independent of endogenous IL-1alpha.
- Antioxidant treatment and NAD(P)H oxidase inhibition significantly reduced MCP-1 production.
- Inhibition of p38 MAP kinase, JNK, NF-kappaB, and AP-1 substantially attenuated MCP-1 expression.
- Activation of NF-kappaB and AP-1 was confirmed in P. gingivalis-infected HUVEC.
Conclusions:
- P. gingivalis infection upregulates MCP-1 expression in endothelial cells.
- The upregulation is mediated by reactive oxygen species (ROS) and involves the activation of p38 MAP kinase, JNK, NF-kappaB, and AP-1 signaling pathways.
