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Gallbladder mucosal protein secretion during development of experimental cholecystitis
D L Kaminski1, Y G Deshpande, A Li
1Department of Surgery, St. Louis University Hospital, Missouri 63110-0250, USA.
Digestive Diseases and Sciences
|May 1, 1995
Summary
Lysophosphatidylcholine induces gallbladder distension in cholecystitis by promoting an active secretory process for albumin accumulation, rather than direct cell damage. This finding clarifies the mechanism of protein buildup in the gallbladder during inflammation.
Area of Science:
- Gastroenterology
- Cell Biology
- Pathophysiology
Background:
- Experimental cholecystitis involves altered gallbladder mucosa absorptive characteristics.
- Lysophosphatidylcholine (LPC) causes intraluminal accumulation of water, glycoprotein, and protein.
Purpose of the Study:
- To determine if LPC-induced protein accumulation in the gallbladder lumen is due to cytolysis or active secretion.
- To characterize the specific protein accumulating in the gallbladder during experimental cholecystitis.
Main Methods:
- Gallbladder perfusion experiments in anesthetized cats with and without LPC.
- Measurement of perfusate protein and calculation of albumin clearance with vesicular transport inhibitors.
- SDS-PAGE and immunoblotting to identify the secreted protein.
Main Results:
- Inhibitors of microtubular and microfilament activity reduced LPC-induced protein accumulation and albumin clearance.
- LPC significantly increased perfusate lactate dehydrogenase (LDH) levels.
- The accumulating protein was identified as albumin (approximately 66-kDa).
Conclusions:
- LPC induces albumin accumulation in the gallbladder via an active secretory process, not solely cytolysis.
- This active secretion contributes to gallbladder distension during cholecystitis development.
- Cellular transport mechanisms are involved in LPC-induced protein leakage.