Helicobacter pylori lipopolysaccharides preferentially induce CXC chemokine production in human monocytes

Helicobacter pylori infection can cause duodenal ulcers and may also induce gastric adenocarcinoma. The bacteria colonize the gastric mucosa and areas of gastric metaplasia in the duodenum for decades, resulting in active chr onic inflammation in the infected areas, A characteristic feature of the in fection is the ongoing recruitment of neutrophils to the infected sites. To evaluate the role of H. pylon lipopolysaccharides (LPS) in the recruitment of leukocytes to the gastric mucosa, we have examined the cytokine and che mokine production from human monocytes stimulated with LPS isolated from di fferent H. pylori strains, as well as from several other gram-negative bact eria, Our results show that H, pylori LPS induce a large production of neut rophil-recruiting CXC chemokines (interleuin-8 and growth-related oncogene alpha) from purified human monocytes, to almost the same extent as Escheric hia coli LPS, However, and in agreement with previous studies, H. pylori LP S was much less potent in inducing production of proinflammatory cytokines by purified human monocytes and was also a weak inducer of the CC chemokine RANTES. There was no difference between LPS preparations from different H, pylori strains in their ability to induce cytokines and chemokines, The pr eferential production of CXC chemokines after stimulation with H, pylori LP S indicates an important contribution of this molecule in maintaining neutr ophil recruitment during the infection, irrespective of the infecting strai n.