Helicobacter pyloriLipopolysaccharides Preferentially Induce CXC Chemokine Production in Human Monocytes

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Abstract
Helicobacter pyloriinfection 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 chronic inflammation in the infected areas. A characteristic feature of the infection is the ongoing recruitment of neutrophils to the infected sites. To evaluate the role ofH. pylorilipopolysaccharides (LPS) in the recruitment of leukocytes to the gastric mucosa, we have examined the cytokine and chemokine production from human monocytes stimulated with LPS isolated from differentH. pyloristrains, as well as from several other gram-negative bacteria. Our results show thatH. pyloriLPS induce a large production of neutrophil-recruiting CXC chemokines (interleukin-8 and growth-related oncogene alpha) from purified human monocytes, to almost the same extent asEscherichia coliLPS. However, and in agreement with previous studies,H. pyloriLPS 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 differentH. pyloristrains in their ability to induce cytokines and chemokines. The preferential production of CXC chemokines after stimulation withH. pyloriLPS indicates an important contribution of this molecule in maintaining neutrophil recruitment during the infection, irrespective of the infecting strain.