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Lipopolysaccharide from escherichia coli stimulates mucin secretion by cultured dog gallbladder epithelial cells
Author(s) -
Choi JaeWoon,
Klinkspoor J. Henri,
Yoshida Tadashi,
Lee Sum P.
Publication year - 1999
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510290515
Subject(s) - mucin , secretion , lipopolysaccharide , lactate dehydrogenase , biology , microbiology and biotechnology , chemistry , endocrinology , biochemistry , enzyme
Biliary infection is associated with mucin hypersecretion by the biliary epithelium. Mucins have been identified as potent pronucleators of cholesterol in bile. The aim of the present study was to determine whether lipopolysaccharides (LPS) from different bacteria are capable of stimulating mucin secretion by cultured dog gallbladder epithelial (DGBE) cells, and to investigate the mechanism by which LPS stimulate mucin secretion. Mucin secretion by confluent monolayers of DGBE cells was quantified by measuring the secretion of [3H]‐ N ‐acetyl‐ d ‐glucosamine–labeled glycoproteins. Cell viability was evaluated by measuring the leakage of the enzyme, lactate dehydrogenase (LDH), into the culture medium. LPS, derived from Escherichia coli , Klebsiella pneumoniae ,and Pseudomonas aeruginosa (200 μg/mL), all caused an increase in mucin secretion by the DGBE cells, without causing concomitant cell lysis. LPS from E. coli was found to be the most potent stimulator of mucin secretion, and increased mucin secretion by the DGBE cells to 252% ± 14% of control. LPS from E. coli had no effect on intracellular cyclic adenosine monophosphate (cAMP) levels in the DGBE cells. Addition of the nitric oxide (NO)‐releasing compound, NOR‐4 (0.125‐1 mmol/L), to the cells did not result in increased mucin secretion, and the NO synthase inhibitor, N ω ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME) (4 or 10 mmol/L), did not inhibit the LPS‐stimulated mucin secretion. Exogenous tumor necrosis factor α (TNF‐α) (1‐10 ng/mL) did cause a minor increase in mucin secretion by the DGBE cells, but the effect of LPS from E. coli on mucin secretion could not be inhibited by preincubation with a TNF‐α antibody (10 μg/mL). We conclude that LPS stimulates mucin secretion by the gallbladder epithelium. Whether this stimulation is mediated by TNF‐α remains to be determined.(Hepatology 1999;29:1352‐1357.)