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β 1 ‐Adrenoceptor antibody‐induced increase in soluble CD40 ligand release in chronic periodontitis patients: role of prostaglandin E 2
Author(s) -
SterinBorda Leonor,
Segovia Marcela,
Reina Silvia,
Borda Enri
Publication year - 2012
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2012.065748
Subject(s) - prostaglandin e , chemistry , antibody , prostaglandin , autoantibody , atenolol , extracellular , endocrinology , medicine , lactate dehydrogenase , prostaglandin e2 , periodontitis , biochemistry , enzyme , immunology , blood pressure
In this paper, we demonstrate that circulating antibodies from chronic periodontitis patients reacting with atrial β 1 ‐adrenoceptors (β 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 β 1 synthetic peptide (with an amino acid sequence identical to the second loop of human myocardial β 1 ‐ARs) as a coating antigen, we demonstrated reactivity against the second extracellular loop on human myocardial β 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 β 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 β 1 ‐AR antibodies.