Expression of the Adhesion Molecules Mac-1 and l-Selectin on Neutrophils in Acute Pancreatitis is Protease- and Complement-Dependent

Abstract

Trypsin-generated complement activation participates in the upregulation of Mac-1 and shedding of L-selectin on neutrophils in acute pancreatitis. Protease or complement inhibition may be effective in preventing leukocyte migration and subsequent local and remote organ injury.