STUDIES ON THE ETIOLOGY OF ACUTE ACALCULOUS CHOLECYSTITIS - THE EFFECT OF LIPOPOLYSACCHARIDE ON HUMAN GALLBLADDER MUCOSAL CELLS

Previous studies in animals have shown that lipopolysaccharide produce s experimental cholecystitis possibly through a platelet-activating fa ctor-prostanoid mediated process. In this study it was intended to eva luate the effect of LPS on primary cultures of human gallbladder mucos al cells. Gallbladder mucosal cells were isolated from gallbladders re moved during routine cholecystectomies or other operations. The cells were cultured for 24 h before treatment. Unstimulated cells produced l ow levels of prostanoids and significant basal levels of PAF. LPS prod uced stimulation of eicosanoid and PAF secretion. The increased prosta noid formation was not enhanced when LPS and PAF were administered tog ether Prostanoid synthesis was inhibited by the administration of a cy clooxygenase inhibitor while administration of a PAF receptor antagoni st significantly increased prostanoid formation, suggesting that incre ased PAF levels function as a negative control mechanism to decrease p rostanoid synthesis. The results suggest that endotoxemia may produce a cascade of inflammatory processes in human gallbladder mucosal cells resulting in the development of acute acalculous cholecystitis.