EVIDENCE FOR, AND CHARACTERIZATION OF, A LIPOPOLYSACCHARIDE-INDUCIBLEADENOSINE A2 RECEPTOR IN HUMAN TRACHEAL GLAND SEROUS CELLS

Human tracheal glands are considered as the principle secretory struct ures in the bronchotracheal tree. In earlier studies, we successfully performed primary cultures of human tracheal gland (HTG) serous cells and noted that these cells were responsive to many secretagogues inclu ding purinergic agonists but not to the inflammatory mediator adenosin e. In this study, we demonstrate that adenosine was capable of inducin g stimulation of protein secretion by HTG serous cells which had previ ously been cultured in pro-inflammatory conditions (induced by Lipopol ysaccharide (LPS)). This stimulation was inhibited by 8-phenyltheophyl line but not by dipyridamole, which is indicative of a P1 purinoceptor . This inducible receptor is of the adenosine A2 subtype [rank potency order: 5'-(N-ethyl)-carboxamidoadenosine (NECA) > adenosine > N-6-(ph enylisopropyl)-adenosine (PIA); and stimulation of adenylyl cyclase]. The adenosine-induced protein secretion was concentration-dependent, h owever, increased intracellular cyclic adenosine monophosphate (cAMP) was not dependent oo the concentration of adenosine. The adenosine-ind uced secretion and the ATP-induced secretion were shown to be additive . This study concludes that there is evidence of a LPS-inducible adeno sine A2 receptor in human tracheal gland serous cells.