Autoantibodies to β₁‐adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger prostaglandin E₂ generation

Abstract

This article supports the participation of humoral immune alterations in chronic periodontal disease resulting in postsynaptic functional deregulation. Overproduction of proinflammatory mediators (PGE(2) and CD40 expression) is induced as a consequence of antibody-beta(1)-AR interaction. The PGE(2)-CD40-IgG axis may play a part in the pathophysiological mechanisms underlying the inflammatory process in chronic periodontal disease.

Proliferation in cardiac fibroblasts induced by β1-adrenoceptor autoantibody and the underlying mechanisms

“…However, the excessive extracellular matrix deposition contributes to cardiac dysfunction. A previous research suggested β 1 -AA induced fibroblast CD40 and triggered prostaglandin E2 generation35. Our results indicated that conditioned medium of cardiac fibroblasts treated with β 1 -AA changed the secretion of cardiac fibroblasts, which promote apoptosis of cardiomyocytes.…”

“…It has been reported that β 1 -AR was expressed in cardiac fibroblasts27. In addition, it has been reported that β 1 -AA induced the overexpression of fibroblast CD40 and trigger generation of protaglandin E23536. Here we put forward thatβ 1 -AA activated β 1 -AR in cardiac fibroblasts.…”

Autoantibodies to theβ1-Adrenoceptor from Patients with Periodontitis as a Risk Factor for Cardiac Dysfunction

“…The serum was separated by centrifugation at 2000 × g and stored at −20°C until used in assays. IgG was obtained by precipitation followed previous reports [17, 18]. …”

“…The IgG fraction was loaded on the affinity column equilibrated with phosphate-buffered saline (PBS) according to previous reports [16, 17]. …”

“…Initial studies of autoimmunity in the pathogenesis of periodontal disease focused on detection of autoantibodies directed towards various self-antigens [13–15], such as autoantibodies against human gingival fibroblasts [16, 17]. Specifically, these antigingival fibroblast autoantibodies could interact with β 1 -ARs exhibiting adrenergic agonistic activity.…”