The effect of butyric acid on adhesion molecule expression by human gingival epithelial cells

Takigawa, Satoko; Sugano, Naoyuki; Nishihara, Reiko; Koshi, Ryosuke; Murai, Masakazu; Yoshinuma, Naoto; Ochiai, Kuniyasu; Ito, Koichi

doi:10.1111/j.1600-0765.2007.01048.x

Cited by 17 publications

(30 citation statements)

References 35 publications

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“…Butyric acid disrupts human cell adhesion and contributes to tissue damage in periodontal disease caused by Gram-negative anaerobes (9,15). This suggests that butyric acid in periodontal pockets disrupts the tight attachment of epithelial cells, resulting in bacterial penetration and periodontal tissue destruction.…”

Section: Discussionmentioning

confidence: 99%

“…High concentrations of butyric acid have been found in the dental plaque of periodontitis patients (10)(11)(12)(13)(14). Takigawa et al demonstrated that butyric acid significantly decreased viability of epithelial cells in a dose-dependent manner and induced ICAM-1 expression (15). Therefore, we postulate that the inhibition of the action of butyric acid on the epithelium reduces the pathogenicity of Gram-negative anaerobes.…”

Section: Introductionmentioning

confidence: 94%

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Effects of sodium bicarbonate on butyric acid-induced epithelial cell damage in vitro

et al. 2008

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Butyric acid is detected in periodontalpockets and is thought to be involved in the initiation and progression of periodontal disease. We examined the effects of sodium bicarbonate on the butyric acidinduced epithelial cell damage. The human gingival carcinoma cell line Ca9-22 was cultured in medium that contained butyric acid with or without sodium bicarbonate. The viability of cells treated with sodium bicarbonate was significantly higher than that of cells treated with butyric acid alone. The effects of butyric acid on ICAM-1 expression were significantly improved by sodium bicarbonate. Within the limitations of this in vitro study, sodium bicarbonate was indicated to be a useful therapeutic agent to reduce the butyric acidinduced periodontal tissue damage. (J. Oral Sci. 50, [413][414][415][416][417] 2008)

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

Effects of sodium bicarbonate on butyric acid-induced epithelial cell damage in vitro

et al. 2008

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“…Taken together, it seems that butyrate and other SCFA are virulence factors in periodontal disease.Butyrate can activate the free fatty acid receptor-2 (FFAR2), also known as G-protein coupled receptor-43 (GPR43) [20], but also inhibit the histone deacetylase (HDAC) [21]. Using either of these mechanisms, butyrate reduces proliferation and induces apoptosis in gingival fibroblast [22][23][24][25], stimulates T-cell apoptosis [26] and osteoblast maturation [27], as well as pro-inflammatory cytokine release by neutrophils [28]. Butyrate also reduced integrin expression in Ca9-22 epithelial cells [23,29] and promoted autophagy [30].…”

mentioning

confidence: 99%

“…Using either of these mechanisms, butyrate reduces proliferation and induces apoptosis in gingival fibroblast [22][23][24][25], stimulates T-cell apoptosis [26] and osteoblast maturation [27], as well as pro-inflammatory cytokine release by neutrophils [28]. Butyrate also reduced integrin expression in Ca9-22 epithelial cells [23,29] and promoted autophagy [30]. The presence of SCFA in the infectious site attenuates the neutrophils response to A. actinomycetemcomitans as a result of the inhibition of specific isoforms of HDACs, namely, HDAC 1 and 3, but not activation of FFAR2 [31].…”

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confidence: 99%

Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells

Magrin

Summa

Strauß

et al. 2020

IJMS

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Short-chain fatty acids (SCFA) are bacterial metabolites that can be found in periodontal pockets. The expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) within the epithelium pocket is considered to be a key event for the selective transmigration of leucocytes towards the gingival sulcus. However, the impact of SCFA on ICAM-1 expression by oral epithelial cells remains unclear. We therefore exposed the oral squamous carcinoma cell line HSC-2, primary oral epithelial cells and human gingival fibroblasts to SCFA, namely acetate, propionate and butyrate, and stimulated with known inducers of ICAM-1 such as interleukin-1-beta (IL1β) and tumor necrosis factor-alfa (TNFα). We report here that butyrate but not acetate or propionate significantly suppressed the cytokine-induced ICAM-1 expression in HSC-2 epithelial cells and primary epithelial cells. The G-protein coupled receptor-43 (GPR43/ FFAR2) agonist but not the histone deacetylase inhibitor, trichostatin A, mimicked the butyrate effects. Butyrate also attenuated the nuclear translocation of p65 into the nucleus on HSC-2 cells. The decrease of ICAM-1 was independent of Nrf2/HO-1 signaling and phosphorylation of JNK and p38. Nevertheless, butyrate could not reverse an ongoing cytokine-induced ICAM-1 expression in HSC-2 cells. Overall, these observations suggest that butyrate can attenuate cytokine-induced ICAM-1 expression in cells with epithelial origin.Int. J. Mol. Sci. 2020, 21, 1679 2 of 15 crevicular fluid by means of a tightly controlled expression of adhesion molecules, thereby defending microbiological antagonism in the periodontal tissue [2,3]. Thus, the increase of adhesion molecules by inflammatory mediators has to be counterbalanced by local cues to control an excessive influx of cells of the innate immune system.The influx of cells is controlled by intercellular adhesion molecule-1 (ICAM-1), allowing the transmigration of leucocytes which express the corresponding lymphocyte function-associated antigen-1 and macrophage adhesion ligand-1 [4]. ICAM-1, being induced by inflammatory cues such as interleukin-1-beta (IL1β) and tumor necrosis factor-α (TNFα) [5], is expressed by the vascular endothelium and by the junctional epithelium [6], thus, facilitating transmigration of leukocytes across vascular endothelia and the invasion of the extracellular matrix [7]. Although ICAM-1 is consistently expressed by junctional epithelial cells in healthy gingiva and in pocket epithelium, it is not detectable on the majority of keratinocytes in the external gingival epithelium [6,8]. The question then arises, how is the expression of ICAM-1 in epithelial cells controlled?The increase of ICAM-1 expression by inflammatory cues is evidently well-documented. Inflammatory mediators including IL-6 and prostaglandin E 2 increase ICAM-1 expression in human oral squamous cell carcinoma SCC4 cells in vitro [9,10]. Primary gingival epithelial cells increasingly express ICAM-1 upon inflammatory cytokines stimuli, namely, TNFα and interferon-γ [11]....

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“…gingivalis can secrete butyric acid, which affects adhesion molecules in gingival epithelial cells (23). Lipopolysaccharide (LPS), a well-known virulent factor, stimulates proinflammatory cytokines, osteoclast, and bone, resulting in oral diseases (24).…”

Section: Introductionmentioning

confidence: 99%

Identification of Bacteria Associated with a Periodontal Disease in Thai Patients Based on Next-Generation Sequencing

Payungporn

Arirachakaran

Poomipak

et al. 2017

Jundishapur J Microbiol

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The effect of butyric acid on adhesion molecule expression by human gingival epithelial cells

Abstract: The results of the present study indicate that butyric acid alters the expression of adhesion molecules by Ca9-22 cells. The elucidation of the mechanism of action of butyric acid on the periodontium may help to clarify several aspects of the onset and progression of periodontal disease.

Cited by 17 publications

References 35 publications

Effects of sodium bicarbonate on butyric acid-induced epithelial cell damage in vitro

Effects of sodium bicarbonate on butyric acid-induced epithelial cell damage in vitro

Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells

Identification of Bacteria Associated with a Periodontal Disease in Thai Patients Based on Next-Generation Sequencing

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