歯周病原性細菌のLPS刺激によるB細胞内チロシンリン酸化の解析
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Specific gram-negative subgingival bacteria including Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans have been implicated in the pathogenesis of periodontal diseases. These microorganisms possess endotoxic lipopolysaccharides (LPS) as a membrane component, immunological potencies of which may contribute to the inflammatory reaction in periodontal tissues. Since histopathological studies demonstrated that the localized and chronically inflamed gingival tissues of the patients with periodontitis are characterized as hyper-B-cell lesions in which increased numbers of plasma cells occur, the LPS of the organisms could be a potent stimulator of immunological responses by the immunocompetent cells, especially B lymphocytes. Despite the importance of the LPS-B lymphocytes interaction, the molecular mechanism such as tyrosine protein phosphorylation which is thought to be a part of the signal transduction mechanism that mediates later cellular responses, has not been fully understood. We have previously reported that P. gingivalis LPS (PgLPS) increased tyrosine phosphorylation on the substrate proteins that uncluded the phosphoproteins with apparent molecular masses of 24.8 and 26.0kDa (p24.8 and p26.0) in the splenic B lymphocytes from LPS-responsive C3H/HeN and LPS-hyporesponsive C3H/HeJ mice. In this study, the further nature of LPS-induced tyrosine phosphorylation in B lymphocytes using A. actinomycetemcomitans LPS (AaLPS) as well as PgLPS was examined. When detected under Western blot analysis by using the monoclonal anti phosphotyrosine antibody, AaLPS as well as PgLPS and the LPS from Escherichia coli (EcLPS) induced p24.8 and p26.0 in the B lymphocytes from C3H/HeN mice. In the B lymphocytes from C3H/HeJ mice, however, only a trigger signal by PgLPS could be induced to initiate tyrosine protein phosphorylation. Furthermore, lipid A from Salmonella minnesola R595 also induced p24.8 and p26.0 in the B lymphocytes from C3H/HeN mice, suggesting that the lipid A moiety of LPS could be potent for the LPS-induced tyrosine phosphorylation in B lymphocytes. The treatment with herbimycin A as well as genistein abrogated the LPS-induced tyrosine phosphorylation and the proliferative response of B lymphocytes. These findings strongly suggested that increased tyrosine protein phosphorylation in B lymphocytes following the stimulation with LPS from either periodontopathic bacteria could be an important signaling event that might lead to cellular responses. However, no obvious effect has been observed by treatment with a phosphatase inhibitor. In addition, increased serine/threonine protein phosphorylation in B lymphocytes could be also an important signaling event, since the proliferative response of B lymphocytes following LPS stimulation was inhibited by the preincubation of the cells with a serine/threonine kinase inhibitor, staurosporine. Taken together, the present findings suggest that periodontopathic bacteria including A. actinomycetemcomitans and P. gingivalis have a potent property to induce the stimulation of B lymphocytes by the lipid A moiety, in which increased tyrosine protein phosphorylation followed by other protein phosphorylations could be important signaling events that might lead to cellular responses.
- 福岡歯科大学学会の論文
- 1998-03-31
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