Evaluation of the role of prostaglandins E and F in human cholecystitis.

The role of chemical mediation by arachidonic acid metabolites of inflammation in human cholecystitis was evaluated by comparing gallbladder PGE and PGF formation to the degree of inflammation present. Twenty-five human gallbladders containing stones were operatively removed. A strip of fundus was used for histologic evaluation. In a blinded fashion, three pathologists quantitated the amount of inflammation present using a histologic scoring system. Gallbladder mucosal cells were separated from muscle wall by submucosal injection of EDTA and shaking in tissue culture media. Separated mucosal cells and finely minced muscle wall were maintained in tissue culture medium for 3 hours. Hourly PGE and PGF levels in media (extracellular) and mucosal cell and muscle tissue homogenate (intracellular) PGE and PGF concentrations were determined by radioimmunoassay. PGE production increased by both mucosal cell and muscle tissue with increasing inflammation. A significant positive linear correlation existed between the histologic score of inflammation and PGE production by gallbladder mucosal cells and muscle tissue. No correlation existed between the amount of inflammation present and PGF production by mucosal cells or muscle tissue. The results demonstrate an increase in PGE production by human gallbladder tissue with increasing inflammation and suggest that arachidonic acid metabolites may be important mediators of the inflammatory process in human cholecystitis.