Intestinal permeability in a healthy subjects in developing country (Brazil)

Abstract

nism of LPC-induced mucus glycoprotein secretion in the gallbladder (GB) epithelial cells (EC). METHODS: Mucus glycoprotein secretion was studied using cultured dog GBEC (Lab Invest 64:682,1991). PG E2 and 6-ketoPG Fl oin media was assayed by ELISA. Intracellular calcium ([Ca2+]i) was assayed by fluorecent dye method using Fra-2. Effects of LPC (50p,M) on PG synthesis and mucus glycoprotein secretion with or without various inhibitors of arachidonic acid cascades or calcium chelator (EDTA) were examined. Effects of calcium ionophore (ionomycin) or PKC-activator (PMA) on the mucin secretion was also studied. RESULTS: LPC significantly promoted mucus glycoprotein secretion in GBEC. This was associated with increases in PG E2_ and 6keto-PG FI_aproduction as well as in [Caz+]i. Treatment with cyclooxygenase inhibitor (indomethacin) or phospholipase A2 inhibitors (DEPA, OBAA) partially inhibited the LPC-induced mucin secretion. Treatment with Caz+ chelator (EGTA) also partially inhibited the LPC-induced mucin secretion. Calcium ionophore (ionomycin) and calcium-dependent PKC-activator (PMA) both induced the mucus glycoprotein secretion. CONCLUSIONS: Gallbadder mucus glycoproten secretion is mediated by both arachidonic acid cascade and calcium-dependent pathway. LPC promotes mucus glycoprotein secretion by activating both pathways.