β1-Adrenoceptor antibody-induced increase in soluble CD40 ligand release in chronic periodontitis patients: Role of prostaglandin E2

Abstract

In this paper, we demonstrate that circulating antibodies from chronic periodontitis patients reacting with atrial β1-adrenoceptors (β1-ARs) act as an inducer of soluble CD40 ligand (sCD40L) release and prostaglandin E2 (PGE2) generation. By enzyme-linked immunosorbent assay using β1 synthetic peptide (with an amino acid sequence identical to the second loop of human myocardial β1-ARs) as a coating antigen, we demonstrated reactivity against the second extracellular loop on human myocardial β1-ARs. This autoantibody present in the serum of chronic periodontitis patients was significantly correlated with the release of sCD40L and PGE2. The release of sCD40L was blunted by atenolol, SP600125 and β1 synthetic peptide, and PGE2 generation was inhibited by DuP 697 and slightly by FR122049. The effects of the antibody incubated with isolated rat atria upregulated sCD40L release with an increase of PGE2 production and c-Jun N-terminal kinase phosphorylation. These results indicate that in chronic periodontitis patients, there is a positive association between sCD40L release and PGE2 generation via the action of β1-AR antibodies.