Up-regulation of ICAM-1/VCAM-1 promotes the progression of periodontitis by activating the NF-κB pathway

Periodontitis remains to be one of the most common oral diseases, and brings huge damage to people's life. Inflammations play significant roles in the biology of periodontitis. This study was aimed to investigate the highly expressed proteins of ICAM-1 and VCAM-1 in the development of periodontitis at the inflammatory level and to reveal its possible mechanism. Expression of the targets in the inflamed gingiva-isolated periodontal lymphocytes and normal lymphocytes was measured. The effects of ICAM-1 and VCAM-1 expression on periodontal lymphocytes apoptosis were analyzed. Furthermore, the cell apoptosis-and signal pathway-related protein expression were also analyzed. Compared to the normal lymphocytes, ICAM-1 and VCAM-1 were highly expressed in periodontal lymphocytes. When cells were treated with the ICAM-1/VCAM-1 antibody, the cell apoptosis was enhanced compared to the controls and this effect was more apparent when cells were treated with the two antibodies. Besides, Bcl-2 and Bcl-xs expression was both significantly increased by the suppressed ICAM-1/VCAM-1, whereas the p-IKB alpha and p-IKK alpha/beta levels were significantly decreased. Similarly, the decreased effects of the suppressed ICAM-1/VCAM-1 on the former proteins expression were more apparent when cells were treated with the two antibodies. Taken together, our study revealed that the overexpressed ICAM-1/VCAM-1 may contribute to the development and progression of periodontitis through inhibiting apoptosis and activating the NF-kappa B signal pathway.