Abstract
We have examined the responses of polymorphonuclear neutrophils (PMNs) and human umbilical vein endothelial cells (HUVEC) to Helicobacter pylori lipopolysaccharides (LPSs). High-antigenicity-polysaccharide-carrying smooth LPS and rough LPS from H. pylori were used for the experiments. PMN activation was determined by chemiluminescence response (CLR). The priming effect of patient's serum or IL-8 on the CLR was also examined. After stimulation of HUVEC with the LPSs, the supernatant was tested for IL-6, IL-8 and RANTES by ELISA. Direct induction of CLR was observed after the stimulation of H. pylori LPSs. Though the response was weak, enhancement occurred in response to high-antigenicity-polysaccharide-carrying smooth LPS by patient's serum against the LPS. IL-8 priming was also effective to enhance CLR, which was induced by H. pylori LPS. Following exposure to H. pylori LPSs, HUVEC secreted IL-6 and IL-8 but not RANTES. The enhanced secretion of both IL-6 and IL-8 occurred in a time-dependent manner. However, the cytokine-inducing ability of H. pylori LPSs is significantly lower than that of other Gram-negative bacteria such as Escherichia coli and Campylobacter jejuni. Structurally similar LPS from Porphyromonas gingivalis also showed weak potency. These results suggest that the ability of H. pylori LPSs is not directly effected to induce inflammation. However, an indirect effect of these LPSs, or continuous stimulation with these LPSs to endothelial cells, may relate to persistent infection.
