IL-1β enhances cell adhesion through laminin 5 and β4 integrin in gingival epithelial cells

Abstract

The junctional epithelium and dental enamel adhere because of hemidesmosomes containing laminin 5 and α6β4 integrin, which are important adhesion molecules in the internal basal lamina. Interleukin (IL)-1 is important in the pathogenesis of periodontal disease. IL-1β induces bone resorption by activating osteoclasts; however, its effects on adhesion of epithelial cells remain to be clarified. Laminin β3, β4 integrin, and focal adhesion kinase mRNA levels were higher after 1 h and 3 h of stimulation with IL-1β (1 ng/mL), and IL-1β, type I α1, and type IV α1 collagen mRNA levels were higher after 1 h and lower after 3 h of stimulation with IL-1β. After IL-1β stimulation, colocalization of laminin 5 and β4 integrin was increased after 1 h, colocalization of β4 integrin and plectin was increased after 1 h and decreased after 3 h, and colocalization of β4 integrin and type IV collagen was decreased after 3 h. Wound healing assays showed that IL-1β treatment (3 h) delayed wound healing. These results suggest that IL-1β enhances cell adhesion by altering localization of epithelial adhesion molecules.

Macrophage migration inhibitory factor regulates specific innate immune sensor responses in gingival epithelial cells

“…The effect of MIF deficiency on IL-1R expression was investigated, providing the essential role of IL-1β in the regulation of tissue homeostasis and IL-8/CXCL8 expression. [28][29][30] Initially, it was found that mRNA for both isoforms of the IL-1 receptor (IL-R1 and IL-R2) were strongly expressed in primary GECs (Figure 6A). Inhibition of MIF significantly reduced the expression of both IL-1R1 and IL-1R2 (Figure 6B).…”