Effects of Actin Polymerization on Cellular Adhesion Induced by CXCL12

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Periodontal diseases are chronic inflammatory diseases caused by pathogenic bacteria in dental plaque, characterized by complex interactions among fibroblasts and immunocompetent cells, such as T cells. In T cells, Ig superfamily members activate tyrosine kinases to activate integrins. The role of chemokine stimulation has not been clarified. Therefore, we used T cell-like Jurkat cells expressing the receptor for stromal cell-derived factor-1α(CXCL12, a CXC chemokine) and investigated adhesion to fibronectin, an extracellular matrix protein and a β1-integrin ligand. The results confirmed that CXCL12 stimulation enhanced adhesion of Jurkat cells to fibronectin with anti -α4, -α5 and β1-integrin antibodies inhibited adhesion to fibronectin. Although CXCL12 stimulation also facilitated actin polymerization, no effects were seen with anti -α4, -α5 or β1-integrin antibodies. The above findings suggest that CXCL12 -induced adhesion of Jurakat cells to fibro-nectin is dependent on integrin activation, and increased adhesion accelerates immune reactions in inflamed tissue.
日本再生歯科医学会の論文
2007-09-30