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Eur J Immunol. 2018 Dec;48(12):1965-1974. doi: 10.1002/eji.201847658. Epub 2018 Oct 22.

Porphyromonas gingivalis triggers NLRP3-mediated inflammasome activation in macrophages in a bacterial gingipains-independent manner.

Author information

1
Department of Bacterial Pathogenesis, Infection and Host Response, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
2
Division of Microbiology and Oral Infection, Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.

Abstract

Porphyromonas gingivalis is a Gram-negative anaerobic bacterium that has been considered to be one of the bacteria associated with progression of human periodontitis. Subgingival biofilms formed by bacteria, including P. gingivalis, induce chronic inflammation, and activation of inflammasome in the gingival tissue. However, the mechanisms of P. gingivalis-triggering inflammasome activation and the role of bacteria-host interactions are controversial. In this study, we investigated the potential of P. gingivalis for triggering inflammasome activation in human cells and mouse models. We demonstrated that secreted or released factors from bacteria are involved in triggering NLR family, pyrin-domain containing 3 protein (NLRP3) inflammasome in a gingipain-independent manner. Our data indicated that released active caspase-1 and mature IL-1β are eliminated by proteolytic activity of secreted gingipains. These results elucidate the molecular bases for the mechanisms underlying P. gingivalis-triggered inflammasome activation.

KEYWORDS:

Caspase-1; NLRP3 inflammasome; NOD-like receptor; Periodontitis; Porphyromonas gingivalis

PMID:
30280383
DOI:
10.1002/eji.201847658
[Indexed for MEDLINE]

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