Abstract
Previous observations suggest that interleukin-1 (IL-1) may play an important role in the progression of periodontitis. In the present study, we investigated whether a cell-associated IL-1 alpha (CAIL-1 alpha) produced in human gingival fibroblasts (HGF) induces biological activities related to the progression of periodontitis. HGF were treated with recombinant human IL-1 beta (rhIL-1 beta) for 12 h. After that, the cell layers of HGF were washed 3 times with fresh medium and were then fixed with 1% paraformaldehyde. The fixed cell layers of HGF were used for assays for bone resorbing activity, prostaglandin E2 (PGE2) production and collagenase activity. Fixed cell layers of HGF treated with rhIL-1 beta enhanced not only calcium release from BALB/c mouse calvaria but also PGE2 production and collagenase activity in HGF and human periodontal ligament fibroblasts (HPLF) cultured on the fixed cell layers. These activities were neutralized by treatment with monoclonal mouse anti-human IL-1 alpha antibody, but monoclonal mouse anti-human IL-1 beta antibody showed no effects on these activities. The induction of these activities by fixed cell layers of HGF required direct contact between the fixed cell layers and the calvaria, HGF, or HPLF. These results suggest that CAIL-1 alpha produced in HGF treated with rhIL-1 beta induces bone resorbing activity, PGE2 production and collagenase activity in the target cells by direct contact; CAIL-1 alpha may play an important role in the progression of periodontitis.
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