Cholinergic Autoantibodies from Primary Sjögren’s Syndrome Modulates Submandibular Gland Na+-K+-ATPase Activity via PGE2 and cAMP

DANIELA PASSAFARO, SILVIA REINA, LEONOR STERIN-BORDA, ENRI BORDA

EUROPEAN JOURNAL OF ORAL SCIENCES

WILEY-BLACKWELL PUBLISHING, INC

Año: 2010 vol. 118 p. 131 - 138

0909-8836

We  demonstrate  that  patients  with  primary  Sjögren’s  syndrome  (pSS)  produce functional  IgG  autoantibodies  that  interact  with  the  glandular  M3  muscarinic acetylcholine  receptors  (mAChRs).  These  autoantibodies  act  as  a  partial muscarinic  agonist,  increasing PGE2  and  cAMP  production modifying Na+-K+-ATPase  activity,  but  also  interfere  with  parasympathetic  neurotransmitter  to secretagogue effect. The IgG from pSS patients has two effects on the submandibular gland. On the one hand, it may act as inducer of the proinflammatory molecule (PGE2) that,  in  turn,  inhibits Na+-K+-ATPase activity. On  the other hand,  it plays a  role  in  the pathogenesis  of  dry mouth,  abolishing  the  Na+-K+-ATPase  inhibition  and  the  net  K+ efflux stimulation of the salivary gland in response to the authentic agonist pilocarpine, decreasing salivary fluid production.