Combined effects of starvation and butyrate on autophagy‐dependent gingival epithelial cell death

Evans, Mark; Murofushi, Takahisa; Tsuda, Hiromasa; Mikami, Yohei; Zhao, Ning; Ochiai, Kuniyasu; Kurita‐Ochiai, Tomoko; Yamamoto, Masafumi; Otsuka, Kichibee; Suzuki, Naoto

doi:10.1111/jre.12418

Cited by 27 publications

(44 citation statements)

References 46 publications

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“…AMPK is a regulator of cellular energy homeostasis, and its activation directly promotes autophagy (Hardie, 2004;Kim, Kundu, Viollet, & Guan, 2011). The exposure of butyrate activated AMPK in GECs (Evans et al, 2017). And then, the activated AMPK inhibited mammalian target of rapamycin complex 1 (mTORC1) which suppressed autophagy signaling (Hardie, 2004).…”

Section: Non-bacterial Autophagymentioning

confidence: 99%

The role of autophagy in the pathogenesis of periodontal disease

Jiang

Zhu

2019

Oral Diseases

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Periodontal disease is a chronic inflammatory disease leading to destruction of periodontal tissues. As a local inflammation, periodontopathic bacterium, pro‐inflammatory mediators, and local immune response play pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease and tooth loss. Autophagy is an intracellular degradation process highly conserved from yeast to humans. As a lysosomal degradation pathway of self‐digestion, it is critical for maintaining cells homeostasis and development. The role of autophagy has been investigated in oral diseases, such as oral cancer, periapical lesions, and oral candidiasis. Recently, increasing studies investigated the role of autophagy in periodontal disease. In this review, we try to illustrate the effect of autophagy on periodontal disease pathogenesis from 5 aspects: autophagy affects the intracellular infection and survival of bacteria; autophagy has an interaction with periodontal inflammation; autophagy is pivotal in periodontal cells biology and periodontal tissues destruction and reconstruction; autophagy can be induced by cigarette smoke; last but not least, autophagy may affect periodontal disease via endoplasmic reticulum stress.

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Section: Non-bacterial Autophagymentioning

confidence: 99%

The role of autophagy in the pathogenesis of periodontal disease

Jiang

Zhu

2019

Oral Diseases

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“…The Ca9-22 cell line was used as an in vitro counterpart of gingival epithelial cells 28 . Bacterial components or chemical regents have previously been reported to induce several inflammatory responses, such as IL-1β, COX-2, and IL-8, in Ca9-22 cells 29,30 .…”

Section: Discussionmentioning

confidence: 99%

“…Bacterial cells were grown anaerobically at 37 °C for 24 h in trypticase soy broth supplemented with yeast extract (1 mg/ml), haemin (5 μg/ml), and menadione (1 μg/ml), as previously described 48 ; they were then used in the following experiments. Ca9-22 cells (originally isolated from human gingival epithelia) were obtained from the Japanese Collection of Research Bioresources (Tokyo, Japan); these cells were used as an in vitro counterpart of gingival epithelial cells 28 because they have been widely used as an in vitro culture model of gingival epithelial cells 28,49 . The cells were cultured in Dulbecco's modified Eagle's medium (DMEM) (Wako, Osaka, Japan) supplemented with 10% fetal bovine serum at 37 °C in 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Porphyromonas gulae and periodontal disease in dogs by a combination of clindamycin and interferon alpha

Nomura

Inaba

Yasuda³

et al. 2020

Sci Rep

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Porphyromonas gulae is a major periodontal pathogen in dogs, which can be transmitted to their owners. A major virulence factor of P. gulae consists of a 41-kDa filamentous appendage (FimA) on the cell surface, which is classified into three genotypes: A, B, and C. Thus far, inhibition of periodontal disease in dogs remains difficult. The present study assessed the inhibitory effects of a combination of clindamycin and interferon alpha (IFN-α) formulation against P. gulae and periodontal disease. Growth of P. gulae was significantly inhibited by clindamycin; this inhibition had a greater effect on type C P. gulae than on type A and B isolates. In contrast, the IFN-α formulation inhibited the expression of IL-1β and COX-2 elicited by type A and B isolates, but not that elicited by type C isolates. Furthermore, periodontal recovery was promoted by the administration of both clindamycin and ifn-α formulation to dogs undergoing periodontal treatment; moreover, this combined treatment reduced the number of fimA genotypes in oral specimens from treated dogs. these results suggest that a combination of clindamycin and ifn-α formulation inhibit P. gulae virulence and thus may be effective for the prevention of periodontal disease induced by P. gulae.

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“…gulae strains were grown anaerobically frozen stocks on blood agar plates (Becton Dickinson Co., Ltd., Tokyo, Japan) for 4–5 days at 37°C, followed by anaerobic subculturing for 24 hr at 37°C in Trypticase soy broth supplemented with yeast extract (1 mg/ml), menadione (1 μg/ml) and hemin (5 μg/ml) using the AnaeroPack ® (Mitsubishi Gas Chemical Co., Inc., Tokyo, Japan). Ca9‐22 cells, originated from human gingival epithelia, were obtained from the Japanese Collection of Research Bioresources (Tokyo, Japan), and has been previously used as an in vitro culture model of gingival epithelial cells (Evans et al, 2017; Inaba et al, 2019; Tada et al, 2019). The cells were cultured in Dulbecco's modified Eagle's medium (DMEM; Wako, Osaka, Japan) supplemented with 10% fetal bovine serum at 37°C in 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Porphyromonas gulae lipopolysaccharide elicits inflammatory responses through toll‐like receptor 2 and 4 in human gingivalis epithelial cells

Inaba

Yoshida

Nomura

et al. 2020

Cellular Microbiology

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Porphyromonas gulae, a Gram‐negative black‐pigmented anaerobe, has been associated with periodontal disease in companion animals and its virulence has been attributed to various factors, including lipopolysaccharide (LPS), protease and fimbriae. Toll‐like receptors (TLRs) recognise pathogen‐associated molecular patterns, such as peptidoglycan, lipids, lipoproteins, nucleic acid and LPS. Following P. gulae infection, some inflammatory responses are dependent on both TLR2 and TLR4. In addition, a recent clinical study revealed that acute and persistent inflammatory responses enhance the expressions of TLR2 and TLR4 in the oral cavity. In this study, we investigated the interaction between P. gulae LPS and human gingivalis epithelial cells (Ca9‐22 cells). P. gulae LPS was found to increase TLR2 and TLR4 mRNA expressions and protein productions, and enhanced inflammatory responses, such as COX2, TNF‐ɑ, IL‐6 and IL‐8. Stimulated Ca9‐22 cells exhibited phosphorylation of ERK1/2 and p38, and their inhibitors diminished inflammatory responses, while knockdown of the TLR2 and/or TLR4 genes with small interfering RNA (siRNA) prevented inflammatory responses. Moreover, p38 and ERK1/2 phosphorylation was decreased in TLR2 and TLR4 gene knockdown cells. These findings suggest that P. gulae LPS activates p38 and ERK1/2 via TLR2 and TLR4, leading to inflammatory responses in human gingival epithelial cells.

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Combined effects of starvation and butyrate on autophagy‐dependent gingival epithelial cell death

Cited by 27 publications

References 46 publications

The role of autophagy in the pathogenesis of periodontal disease

The role of autophagy in the pathogenesis of periodontal disease

Inhibition of Porphyromonas gulae and periodontal disease in dogs by a combination of clindamycin and interferon alpha

Porphyromonas gulae lipopolysaccharide elicits inflammatory responses through toll‐like receptor 2 and 4 in human gingivalis epithelial cells

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