[Effect of Actinomyces viscosus on the production of prostaglandin E2 and thromboxane B2 in macrophages].

Certain species of bacteria have been implicated in the etiology and pathogenesis of periodontal diseases. It has been reported that Actinomyces viscosus (A. viscosus) is associated with gingivitis. On the other hand, it is known that prostaglandin (PG) E2 is one of potent mediators of bone resorption and macrophage is PGE2 producing cell. It has been reported that a number of macrophage is increased in inflamed gingival tissues and that A. viscosus (T14V strain) cells significantly stimulated the arachidonic acid (AA) release and the secretion of PGE2 and thromboxane (TX) B2. Furthermore, the level of PGE2 in inflamed gingival tissues was 18 times higher than that of normal gingiva. In general, it is believed that the rate-limiting step in the production of PGs and TXs is dependent on the release of AA from phospholipids in the cell membrane. However, recent papers suggested that the produced levels of PGE2 and TXB2 were not completely dependent on the amounts of released AA, and the mechanism of rate limiting step and the PGE2 production are still remains to be elucidated. It is known that glucocorticoid, anti-inflammatory steroid, inhibits the AA release from phospholipids of cell membrane. In the present study, in order to clarify the mechanism of PGE2 and TXB2 production by the A. viscosus cells, the effect of addition of glucocorticoid on the levels of PGE2 and TXB2 production were studied. The effects of ionophore A 23187 and zymosan, which were known as agents of macrophage activation but having different action manner, on the relation between the AA release and productions of PGE2 and TXB2 were also comparatively studies.(ABSTRACT TRUNCATED AT 250 WORDS)