HELICOBACTER-PYLORI LIPOPOLYSACCHARIDE CAN ACTIVATE 70Z 3 CELLS VIA CD14/

Helicobacter pylori persistently colonizes the human gastrointestinal tract and is associated with chronic gastritis and, in some cases, pep tic ulcer disease or gastric neoplasms, One factor in the persistence of this organism may be its inability to elicit a strong inflammatory response, Lipopolysaccharide (LPS) is a proinflammatory substance foun d in the cell walls of all gram-negative bacteria, H. pylori LPS has b een found by several different measures to be less active than LPS fro m Enterobacteriaceae, This study addresses the role of CD14 and LPS-bi nding protein in the cellular response to H. pylori LPS, We report tha t H. pylori LPS activates mammalian cells expressing CD14 at much lowe r LPS concentrations than those for control cells not expressing CD14, The maximal activation of CD14-70Z/3 cells by H. pylori LPS also requ ires LPS-binding protein, H. pylori LPS at concentrations as high as 3 0 mu g/ml does not elicit an interleukin-8 (IL-8) response from the ep ithelial cell line SW620 in the presence of CD14; 10 ng of Escherichia coil LPS per mi elicits a maximal IL-8 response, Furthermore, in cont rast to some other types of LPS with little activity, H. pylori LPS do es not inhibit the CD14-70Z/3 cell response to E. coil LPS, From these studies, we conclude that H. pylori LPS, though much less active than E. coil LPS, stimulates cells via CD14.