ID | 61941 |
フルテキストURL | |
著者 |
Urmi, Alam Saki
Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Inaba, Hiroaki
Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Nomura, Ryota
Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Yoshida, Shoko
Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kaken ID
Ohara, Naoya
Department of Oral Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and the Advanced Research Center for Oral and Craniofacial Sciences, Dental School, Okayama University
Kaken ID
publons
researchmap
Asai, Fumitoshi
Department of Pharmacology, School of Veterinary Medicine Azabu University
Nakano, Kazuhiko
Department of Pediatric Dentistry, Osaka University Graduate School of Dentistry
Matsumoto‐Nakano, Michiyo
Department of Pediatric Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kaken ID
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抄録 | Porphyromonas gulae, an animal-derived periodontal pathogen, expresses several virulence factors, including fimbria, lipopolysaccharide (LPS) and proteases. We previously reported that its invasive efficiency was dependent on fimbriae types. In addition, P. gulae LPS increased inflammatory responses via toll-like receptors. The present study was conducted to investigate the involvement of P. gulae proteases in bacterial and host cell biology. Porphyromonas gulae strains showed an ability to agglutinate mouse erythrocytes and also demonstrated co-aggregation with Actinomyces viscosus, while the protease inhibitors antipain, PMSF, TLCK and leupeptin diminished P. gulae proteolytic activity, resulting in inhibition of haemagglutination and co-aggregation with A. viscosus. In addition, specific proteinase inhibitors were found to reduce bacterial cell growth. Porphyromonas gulae inhibited Ca9-22 cell proliferation in a multiplicity of infection- and time-dependent manner. Additionally, P. gulae-induced decreases in cell contact and adhesion-related proteins were accompanied by a marked change in cell morphology from well spread to rounded. In contrast, inhibition of protease activity prevented degradation of proteins, such as E-cadherin, beta-catenin and focal adhesion kinase, and also blocked inhibition of cell proliferation. Together, these results indicate suppression of the amount of human proteins, such as gamma-globulin, fibrinogen and fibronectin, by P. gulae proteases, suggesting that a novel protease complex contributes to bacterial virulence.
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キーワード | coaggregation
haemagglutination
P. gulae
protease
protein degradation
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備考 | This is an Accepted Manuscript of an article published by Wiley.
This is the peer reviewed version of the following article: [Urmi, AS, Inaba, H, Nomura, R, et al. Roles of Porphyromonas gulae proteases in bacterial and host cell biology. Cellular Microbiology. 2021; 23:e13312. https://doi.org/10.1111/cmi.13312], which has been published in final form at [https://doi.org/10.1111/cmi.13312]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages there of by third parties from platforms, services and websites other than Wiley Online Library must be prohibited. |
発行日 | 2021-5-3
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出版物タイトル |
Cellular Microbiology
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出版者 | Wiley
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開始ページ | e13312
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ISSN | 1462-5814
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NCID | AA1136678X
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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論文のバージョン | author
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.1111/cmi.13312
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助成機関名 |
Ministry of Education, Culture, Sports, Science and Technology
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助成番号 | 20H03897
20K09918
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