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Sci Rep. 2017 Sep 18;7(1):11759. doi: 10.1038/s41598-017-12173-1.

Infection of microglia with Porphyromonas gingivalis promotes cell migration and an inflammatory response through the gingipain-mediated activation of protease-activated receptor-2 in mice.

Author information

1
Department of Aging Science and Pharmacology, Faculty of Dental Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
2
OBT Research Center, Faculty of Dental Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
3
Department of Implantology, School of Stomatology, Jilin University, Changchun, 130021, China.
4
Division of Frontier Life Science, Department of Medical and Dental Sciences, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki, 852-8588, Japan.
5
Department of Aging Science and Pharmacology, Faculty of Dental Sciences, Kyushu University, Fukuoka, 812-8582, Japan. nakan@dent.kyushu-u.ac.jp.

Abstract

Despite a clear correlation between periodontitis and cognitive decline in Alzheimer's disease, the precise mechanism underlying the relationship remains unclear. The periodontal pathogen Porphyromonas gingivalis produces a unique class of cysteine proteinases termed gingipains that comprises Arg-gingipain (Rgp) and Lys-gingipain (Kgp). Rgp and Kgp are important in the bacterial mediated host cell responses and the subsequent intracellular signaling in infected cells. In the present study, we attempted to clarify the potential effects of Rgp and Kgp on the cellular activation of brain-resident microglia. We provide the first evidence that Rgp and Kgp cooperatively contribute to the P. gingivalis-induced cell migration and expression of proinflammatory mediators through the activation of protease-activated receptor 2. The subsequent activation of phosphoinositide 3-kinase/Akt and mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase/ERK pathways contributes to cell migration and inflammatory response of microglia.

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