Does bile protect or damage interstitial Cajal-like cells in the human gallbladder?

the etiology of gallstone disease is considered to be multifactorial, including biliary cholesterol hypersecretion, supersaturation and crystallization, stone formation, bile stasis and mucus hypersecretion and gel formation. Gallbladder hypomotility seems to be a key process that triggers the precipitation of cholesterol microcrystals from supersaturated lithogenic bile. the purpose of the current study was to determine whether ICLCs in the gallbladder were influenced by lithogenic bile. Gallbladder specimens were collected from 30 patients (8 males and 22 females) who underwent elective laparoscopic cholecystectomy for symptomatic gallstone disease. The control group consisted of 25 consecutive patients (11 males and 14 females) who received elective treatment for pancreatic head tumors. ICLCs were visualized in paraffin sections of gallbladders using double immunofluorescence protocol with monoclonal c-kit antibodies and mast cell tryptase. Cholesterol, phospholipid and bile acid concentrations were measured in bile samples obtained by needle aspiration from the gallbladder at the time of surgery. The number of ICLCs in the gallbladder wall was significantly lower in the study group than in the control group (3.35 ± 1.23 vs. 7.06 ± 1.82 cell/FOV in the muscularis propria, P < 0.001) and correlated with a significant increase in the cholesterol saturation index. The glycocholic and taurocholic acid levels were significantly elevated in the control subjects compared with the study group. The results suggest that bile composition may play an important role in the reduction of ICLC density in the gallbladder.