Gingival epithelial cell expression of macrophage inflammatory protein-1alpha induced by interleukin-1beta and lipopolysaccharide.

BACKGROUND: Elevated levels of the macrophage inflammatory protein-1alpha (MIP-1alpha) are reported in inflammatory bone diseases including periodontitis. We evaluated the ability of interleukin-1beta (IL-1beta) and bacterial lipopolysaccharides (LPSs) to modulate MIP-1alpha expression in epithelial cells, fibroblasts, and polymorphonuclear leukocytes (PMNs). We also evaluated the effect of MIP-1alpha as an osteoclast activating factor. METHODS: Human gingival epithelial cells and fibroblasts were obtained by primary cell culture. PMNs were isolated from healthy controls. Human MG63 osteosarcoma cells were used as osteoblastic cells. After incubation of each cell type with IL-1beta, Porphyromonas gingivalis LPS, and Actinobacillus actinomycetemcomitans LPS, MIP-1alpha mRNA and secreted protein levels were quantified by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, and immunohistochemistry. The ability of recombinant MIP-1alpha to induce osteoclast formation was determined by tartrate resistant acid phosphatase assay. RESULTS: MIP-1alpha expression in PMNs and gingival epithelial cells was induced by IL-1beta and LPS, but neither induced MIP-1alpha expression in gingival fibroblasts or osteoblastic cells. MIP-1alpha was highly expressed in the basal epithelial layer of inflamed gingiva but not in healthy gingiva. MIP-1alpha induced osteoclast formation at an optimal concentration of 0.05 to 2 ng/ml. CONCLUSIONS: MIP-1alpha expression by gingival epithelial cells may be important in initiating inflammation by facilitating accumulation and activation of leukocytes. The ability of MIP-1alpha to facilitate formation of multinuclear bone cells indicates a possible role in periodontitis-associated bone destruction. These findings indicate MIP-1alpha may play an important role in early and later stages of inflammatory-related periodontitis.

Gingival Epithelial Cell Expression of Macrophage Inflammatory Protein-1α Induced by Interleukin-1ß and Lipopolysaccharide.

BACKGROUND: Elevated levels of the macrophage inflammatory protein-1α (MIP-1α) are reported in inflammatory bone diseases including periodontitis. We evaluated the ability of interleukin-1ß (IL-1ß) and bacterial lipopolysaccharides (LPSs) to modulate MIP-1α expression in epithelial cells, fibroblasts, and polymorphonuclear leukocytes (PMNs). We also evaluated the effect of MIP-1α as an osteoclast activating factor. METHODS: Human gingival epithelial cells and fibroblasts were obtained by primary cell culture. PMNs were isolated from healthy controls. Human MG63 osteosarcoma cells were used as osteoblastic cells. After incubation of each cell type with IL-1ß, Porphyromonas gingivalis LPS, and Actinobacillus actinomycetemcomitans LPS, MIP-1α mRNA and secreted protein levels were quantified by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, and immunohistochemistry. The ability of recombinant MIP-1α to induce osteoclast formation was determined by tartrate resistant acid phosphatase assay. RESULTS: MIP-1α expression in PMNs and gingival epithelial cells was induced by IL-1ß and LPS, but neither induced MIP-1α expression in gingival fibroblasts or osteoblastic cells. MIP-1α was highly expressed in the basal epithelial layer of inflamed gingiva but not in healthy gingiva. MIP-1α induced osteoclast formation at an optimal concentration of 0.05 to 2 ng/ml. CONCLUSIONS: MIP-1α expression by gingival epithelial cells may be important in initiating inflammation by facilitating accumulation and activation of leukocytes. The ability of MIP-1α to facilitate formation of multinuclear bone cells indicates a possible role in periodontitis-associated bone destruction. These findings indicate MIP-1α may play an important role in early and later stages of inflammatory-related periodontitis.