Background Periodontitis is a chronic inflammatory immune response by bacterial induced plaque leading to connective tissue destruction and bone resorption. In recently reported that periodontitis is increasingly being recognized as a risk factor for atherosclerosis. Object Inflammatory chemokines, a family of chemotactic cytokine, are small heparin-binding proteins that direct the movement of circulating leukocytes to site of inflammation and injury. The present study was designed to investigate the inflammatory chemokines expression regulated by Actinobacillus actinomycetemcomitans lipopolysaccharide (A. actinomycetemcomitans LPS), part of the normal flora of the mouth, using Microarray technique. Methods Inflammatory chemokines genes expression profiling was performed in Raw 264.7 cells by analyses of microarray and reverse transcription-polymerase chain reaction (RT-PCR). Results Microarray results showed that the induction of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1), MIP-1, MIP-1, regulated upon activation, normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein-2 (MIP-2), and interferon- inducible protein 10 (IP 10) by A. actinomycetemcomitans LPS was increased to 12.5, 1.53, 9.09, 17.3, 2.82, 16.1, and 18.1 folds at 18 h, respectively. To check these chemokines expression by A. actinomycetemcomitans LPS, we examined gene expressions by RT-PCR, and found that the expression of MIP-1, MIP-1, RANTES, MIP-2, and IP 10 was increased 107.1, 93.6, 106.8, 86.5, and 162.0 folds at 18 h, respectively. Conclusion These results suggest that inflammatory chemokines induced by A. actinomycetemcomitans LPS may be etiologic factors for the development of atherosclerosis and periodontitis may be associated with atherosclerosis.