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Updated: Mar 28, 2026
Isolation and Culture of Primary Human Gingival Epithelial Cells using Y-27632
Published on: November 6, 2021
Azithromycin recovers reductions in barrier function in human gingival epithelial cells stimulated with tumor
Tsuyoshi Miyagawa1, Tsuyoshi Fujita1, Hiromichi Yumoto2
1Department of Periodontal Medicine, Division of Applied Life Science, Institute of Biomedical & Health Sciences, Hiroshima University, Japan.
Objective:
The gingival epithelium plays an important role in protecting against the invasion of periodontal pathogens, and the permeability of gingival epithelial cells has been implicated in the initiation of periodontitis. Azithromycin (AZM) has been used in the treatment of chronic inflammatory airway diseases because it regulates cell-cell contact in airway epithelial cells. Therefore, AZM may also regulate barrier function in gingival epithelial cells. In the present study, we examined the effects of AZM on the permeability of human gingival epithelial cells (HGEC) under inflammatory conditions in vitro.
Materials And Methods:
HGEC were stimulated by tumor necrosis factor-α (TNF-α) in the presence of AZM or p38 MAP kinase and ERK inhibitors. Permeability was assessed based on transepithelial electrical resistance (TER). The expression of E-cadherin, phosphorylated p38 MAP kinase, and ERK was analyzed by Western blotting.
Results:
TNF-α decreased TER in HGEC, and AZM and the p38 MAP kinase and ERK inhibitors recovered this decrease. AZM inhibited the phosphorylation of ERK and p38 MAP kinase in TNF-α-stimulated HGEC. Furthermore, AZM recovered the decrease in E-cadherin expression in HGEC stimulated with TNF-α.
Conclusions:
These results suggested that AZM regulated gingival epithelial permeability through p38 MAP kinase and ERK signaling, and may contribute to suppress the inflammation in gingival tissue.
