Paradoxical role of PGE(2) and cAMP in Actinobacillus actinomycetem-comitants strain Y-4-induced lymphocyte proliferation

An immune mechanism has been suggested in the pathogenesis of periodontal d isease. Actinobacillus actinomycetemcomitants (Aa) has been implicated as o ne of the etiological agents that induces the major immune response togethe r with a dense infliltrate of inflammatory cells. But the exact role of the se immune cells in periodontal disease has not yet been clarified. In this study the T lymphocyte (TL) proliferative response was evaluated after havi ng being exposed to free cell supernatant (SN) from Aa. Aa SN increased TL proliferation. This mitogenic effect of Aa SN was attenuated by pretreating TL with indomethacin (INDO) or acetylsalicilyc acid (ASA) but not by polym yxin B. The inhibitory effect of INDO on cell proliferation was reversed by the addition of prostaglandin E-2 (PGE(2)) to the culture assay. Moreover, when immune cells were exposed to Aa SN they were able to generate PGE(2) at the same time as intracellular levels of cAMP decreased. Both, PGE(2) re lease and decrease accumulation of cAMP in TL were blunted by treated lymph ocytes with INDO. in this paper we demonstrate that cell free SN from Aa in duces a mitogenic effect on murine lymphocytes. The mechanism involves the host's immunecompetent cells and the release of PGE(2) and appears not to b e induced by capsular-like polysaccharide antigen. Results show a paradoxic al mitogenic effect of Aa SN accompanied by increased generation of PGE(2) and decreased production of cAMP by lymphocytes.