Beta 1-Adrenoceptor antibody-induced increase in soluble CD40 ligand release in chronic periodontitis patients: role of prostaglandin E(2)g

STERIN-BORDA L, SEGOVIA M, REINA S, BORDA E.

EXPERIMENTAL PHYSIOLOGY.

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2012 vol. 97 p. 1030 - 1039

0958-0670

In this paper, we demonstrate that circulating antibodies from chronic periodontitis patients reacting with atrial beta(1)-adrenoceptors (beta(1)-ARs) act as an inducer of soluble CD40 ligand (sCD40L) release and prostaglandin E(2) (PGE(2)) generation. By enzyme-linked immunosorbent assay using â(1) synthetic peptide (with an amino acid sequence identical to the second loop of human myocardial beta(1)-ARs) as a coating antigen, we demonstrated reactivity against the second extracellular loop on human myocardial beta(1)-ARs. This autoantibody present in the serum of chronic periodontitis patients was significantly correlated with the release of sCD40L and PGE(2). The release of sCD40L was blunted by atenolol, SP600125 and â(1) synthetic peptide, and PGE(2) 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 PGE(2) 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 PGE(2) generation via the action of beta(1)-AR antibodies.