Serum antibodies to Porphyromonas gingivalis block the prostaglandin E-2 response to lipopolysaccharide by mononuclear cells

The ability of rabbit and monkey immune sera to neutralize prostaglandin E-2 (PGE(2)) production by human monocytes stimulated with lipopolysaccharide (LPS) was examined. CD14-dependent LPS activation of PGE(2) was examined under assay conditions which allowed the comparison of preimmune and immune sera. Serum obtained from rabbits immunized with formalin-fixed Porphyromonas gingivalis cells dramatically reduced the amount of PGE(2) produced in response to LPS obtained from three different strains of P. gingivalis but not that from Escherichia coli or Bacteroides fragilis. In addition, a significant reduction in the mean PGE(2) level was observed in the presence of sera from immunized but not control monkeys employed in a vaccine trial. Immune serum samples from five of nine immunized monkeys were able to reduce LPS-induced production of PGE(2) by greater than 50% compared to that in the corresponding preimmune sera. Immune monkey serum, similar to immune rabbit serum, blocked PGE(2) production in response to P. gingivalis LPS but not E. coli LPS. These data demonstrate that immunization with P. gingivalis whole cells can elicit an antibody response that is able to block the PGE(2) response to LPS. Neutralization of LPS-mediated inflammatory mediator production may account in part for the observed suppression of alveolar bone loss in immunized monkeys.