Irsogladine maleate counters the interleukin-1β-induced suppression in gap-junctional intercellular communication but does not affect the interleukin-1β-induced zonula occludens protein-1 levels in human gingival epithelial cells

Background and Objective: Irsogladine maleate counters gap junctional intercellular communication reduction induced by interleukin‐8 or Actinobacillus actinomycetemcomitans in cultured human gingival epithelial cells. Interleukin‐1β is involved in periodontal disease. Little is known, however, about the effect of interleukin‐1β on intercellular junctional complexes in human gingival epithelial cells. Furthermore, irsogladine maleate may affect the actions of interleukin‐1β. In this study, we examined how interleukin‐1β affected gap junctional intercellular communication, connexin 43 and zonula occludens protein‐1, and how irsogladine maleate modulated the interleukin‐1β‐induced changes in the intercellular junctional complexes in human gingival epithelial cells. Material and Methods: Human gingival epithelial cells were exposed to interleukin‐1β, with or without irsogladine maleate. Connexin 43 and zonula occludens protein‐1 were examined at mRNA and protein levels by real‐time polymerase chain reaction and western blotting, respectively. Gap junctional intercellular communication was determined using the dye transfer method. The expression of zonula occludens protein‐1 was also confirmed by immunofluorescence. Results: Interleukin‐1β decreased connexin 43 mRNA levels, but increased zonula occludens protein‐1 mRNA levels. Irsogladine maleate countered the interleukin‐1β‐induced reduction in gap junctional intercellular communication and connexin 43 levels. However, irsogladine maleate did not influence the increased zonula occludens protein‐1 levels. Conclusion: The effect of interleukin‐1β on gap junctional intercellular communication and tight junctions of human gingival epithelial cells is different. The recovery of gap junctional intercellular communication by irsogladine maleate in the gingival epithelium may be a normal process in gingival epithelial homeostasis.