Outer membrane vesicles derived from Porphyromonas gingivalis induced cell death with disruption of tight junctions in human lung epithelial cells

He, Yuhan; Shiotsu, Noriko; Uchida-Fukuhara, Yoko; Guo, Jiajie; Weng, Yao; Ikegame, Mika; Wang, Ziyi; Ono, Koji; Kamioka, Hiroshi; Torii, Yasuhiro; Sasaki, Akira; Yoshida, Kaya; Okamura, Hirohiko

doi:10.1016/j.archoralbio.2020.104841

Cited by 30 publications

(25 citation statements)

References 44 publications

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“…The gingival epithelium protects the connective and bone tissues from bacterial invasion and thus plays an important role in the innate immune response [ 17 , 18 ]. In the course of periodontal disease, inflammation caused by bacteria leads to the disruption of epithelial tight junctions, which facilitates bacterial invasion [ 19 ]. Translocation of bacteria into the underlying connective tissue promotes a destructive inflammatory response, leading to bone loss [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

A cocoa (Theobroma cacao L.) extract impairs the growth, virulence properties, and inflammatory potential of Fusobacterium nucleatum and improves oral epithelial barrier function

2021

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Fusobacterium nucleatum is associated with many conditions and diseases, including periodontal diseases that affect tooth-supporting tissues. The aim of the present study was to investigate the effects of a cocoa extract (Theobroma cacao L.) on F. nucleatum with respect to growth, biofilm formation, adherence, and hydrogen sulfide (H2S) production. The anti-inflammatory properties and the effect on epithelial barrier function of the cocoa extract were also assessed. The cocoa extract, whose major phenolic compound is epicatechin, dose-dependently inhibited the growth, biofilm formation, adherence properties (basement membrane matrix, oral epithelial cells), and H2S production of F. nucleatum. It also decreased IL-6 and IL-8 production by F. nucleatum-stimulated oral epithelial cells and inhibited F. nucleatum-induced NF-κB activation in monocytes. Lastly, the cocoa extract enhanced the barrier function of an oral epithelial model by increasing the transepithelial electrical resistance. We provide evidence that the beneficial properties of an epicatechin-rich cocoa extract may be useful for preventing and/or treating periodontal diseases.

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Section: Introductionmentioning

confidence: 99%

A cocoa (Theobroma cacao L.) extract impairs the growth, virulence properties, and inflammatory potential of Fusobacterium nucleatum and improves oral epithelial barrier function

2021

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“…Multiple studies have concluded similar findings. Recently, He et al ( 33 ) demonstrated in a mouse model that released OMVs from Pg exerted potent cytotoxic effects on lung epithelial cells; Pg OMVs revealed their ability to induce the apoptosis of lung epithelial cells and disrupt the epithelial barrier system. They concluded from their experimental design that these observations suggest that OMVs deliver their pathogenic factors from the oral cavity to respiratory organs without the direct translocation of Pg itself ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Topical application of Porphyromonas gingivalis into the gingival pocket in mice leads to chronic‑active infection, periodontitis and systemic inflammation

Kim¹,

Bando²,

Chang

et al. 2022

Int J Mol Med

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Porphyromonas gingivalis (Pg) , one of the 'red-complex' perio-pathogens known to play a critical role in the development of periodontitis, has been used in various animal models to mimic human bacteria-induced periodontitis. In order to achieve a more realistic animal model of human Pg infection, the present study investigated whether repeated small-volume topical applications of Pg directly into the gingival pocket can induce local infection, including periodontitis and systemic vascular inflammation in wild-type mice. Freshly cultured Pg was topically applied directly into the gingival pocket of the second molars for 5 weeks (3 times/week). After the final application, the mice were left in cages for 4 or 8 weeks and sacrificed. The status of Pg colony formation in the pocket, gingival inflammation, alveolar bone loss, the expression levels of pro-inflammatory cytokines in the serum and aorta, the presence of anti- Pg lipopolysaccharide (LPS) and gingipain (Kpg and RgpB) antibodies in the serum, as well as the accumulation of Pg LPS and gingipain aggregates in the gingiva and arterial wall were evaluated. The topical application of Pg into the gingival pocket induced the following local and systemic pathohistological changes in mice when examined at 4 or 8 weeks after the final topical Pg application: Pg colonization in the majority of gingival pockets; increased gingival pocket depths; gingival inflammation indicated by the increased expression of TNF-α, IL-6 and IL-1β; significant loss of alveolar bone at the sites of topical Pg application; and increased levels of pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-17, IL-13, KC and IFN-γ in the serum in comparison to those from mice receiving PBS. In addition, the Pg application/colonization model induced anti- Pg LPS and gingipain antibodies in serum, as well as the accumulation of Pg LPS and gingipain aggregates in the gingivae and arterial walls. To the best of our knowledge, this mouse model represents the first example of creating a more sustained local infection in the gingival tissues of wild-type mice and may prove to be useful for the investigation of the more natural and complete pathogenesis of the bacteria in the development of local oral and systemic diseases, such as atherosclerosis. It may also be useful for the determination of a treatment/prevention/efficacy model associated with Pg -induced colonization periodontitis in mice.

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“…In addition, P. gingivalis induces lung damage associated with inflammatory response (Benedyk et al, 2016;Chen et al, 2018). Moreover, P. gingivalis can cause respiratory abnormalities by increasing the release of cytokines as well as proteolytic and hydrolytic enzymes that alter the respiratory epithelium to an infectious scenario (Scannapieco, 1999;He et al, 2020). Therefore, it is also possible that the increase in water content also occurred in response to the greater The findings of cardiac biometrics indicate the absence of myocardial hypertrophy triggered by P. gingivalis, which corroborates previous data in mice (Kaneko et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

A common oral pathogen Porphyromonas gingivalis induces myocarditis in rats

Peron

Prates

Antônio

et al. 2022

J Clinic Periodontology

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Aim: To evaluate whether Porphyromonas gingivalis (P. gingivalis) inoculation could induce cardiac remodelling in rats. Materials and Methods:The study was conducted on 33 Wistar rats, which were distributed in the following experimental groups: not inoculated; inoculated with 1 Â 10 8 CFU/ml of bacteria; inoculated with 3 Â 10 8 CFU/ml of bacteria. The animals were inoculated at baseline and on the 15th day of follow-up. Blood collection was performed at baseline and 60 min after each inoculation. At 29 days, the animals were subjected to echocardiography and at 30 days to haemodynamic studies before sacrificing them.Results: Impact of the bacteria was more evident in rats that received higher P. gingivalis concentration. Thus, 3 Â 10 8 CFU/ml of bacteria increased the rectal temperature and water content in the lung as well as myocardial necrosis and fibrosis. P. gingivalis induced the intensification of DNA fragmentation and increased the levels of malondialdehyde, oxidized proteins, and macrophage expression in the myocardium. These findings were associated with lower LV isovolumetric relaxation time, +dP/dt, -dP/dt, and higher end-diastolic pressure.Conclusions: P. gingivalis bacteraemia is significantly associated with adverse cardiac remodelling and may play a biological role in the genesis of heart failure.

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Outer membrane vesicles derived from Porphyromonas gingivalis induced cell death with disruption of tight junctions in human lung epithelial cells

Cited by 30 publications

References 44 publications

A cocoa (Theobroma cacao L.) extract impairs the growth, virulence properties, and inflammatory potential of Fusobacterium nucleatum and improves oral epithelial barrier function

A cocoa (Theobroma cacao L.) extract impairs the growth, virulence properties, and inflammatory potential of Fusobacterium nucleatum and improves oral epithelial barrier function

Topical application of Porphyromonas gingivalis into the gingival pocket in mice leads to chronic‑active infection, periodontitis and systemic inflammation

A common oral pathogen Porphyromonas gingivalis induces myocarditis in rats

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