BACKGROUND: Bacteria have different characteristics in stimulation of human neutrophils to produce reactive oxygen species (ROS) and chemokines. This study examined the ability of Helicobacter pylori to induce production of ROS and chemokines by human neutrophils. METHODS: H. pylori strains (1.5 x 108 CFU/ml) were cocultured with 5 x 104 neutrophils isolated from healthy subjects. Samples were incubated with human serum with or without IgG antibodies to H. pylori. ROS production was measured using luminol-dependent chemiluminescence (LmCL), and the concentrations of chemokines (IL-8, RANTES, MIP-1alpha and MCP-1) were measured by ELISA. RESULTS: The mean of the highest LmCL (peak height; PH) value stimulated by H. pylori was 3318 in the absence of serum. PH increased to 4687 when incubated with anti-H. pylori antibody-positive sera (p <.001) but antibody-negative sera did not affect LmCL response. The mean final concentration of IL-8 produced in the absence of serum was 142.6 pg/ml. Increased IL-8 production was seen by addition of antibody positive serum (p <.01). IL-8 production was not significantly correlated with production of ROS. On the other hand, H. pylori stimulation did not induce neutrophil production of RANTES, MIP-1alpha or MCP-1. CONCLUSIONS: H. pylori was capable of inducing IL-8 production by human neutrophils, but not C-C chemokines. Production of C-X-C dominant chemokine by neutrophils is consistent with the pathological characteristics of H. pylori-induced gastritis, where persistent neutrophil infiltration is present.
BACKGROUND: Bacteria have different characteristics in stimulation of human neutrophils to produce reactive oxygen species (ROS) and chemokines. This study examined the ability of Helicobacter pylori to induce production of ROS and chemokines by human neutrophils. METHODS:H. pylori strains (1.5 x 108 CFU/ml) were cocultured with 5 x 104 neutrophils isolated from healthy subjects. Samples were incubated with human serum with or without IgG antibodies to H. pylori. ROS production was measured using luminol-dependent chemiluminescence (LmCL), and the concentrations of chemokines (IL-8, RANTES, MIP-1alpha and MCP-1) were measured by ELISA. RESULTS: The mean of the highest LmCL (peak height; PH) value stimulated by H. pylori was 3318 in the absence of serum. PH increased to 4687 when incubated with anti-H. pylori antibody-positive sera (p <.001) but antibody-negative sera did not affect LmCL response. The mean final concentration of IL-8 produced in the absence of serum was 142.6 pg/ml. Increased IL-8 production was seen by addition of antibody positive serum (p <.01). IL-8 production was not significantly correlated with production of ROS. On the other hand, H. pylori stimulation did not induce neutrophil production of RANTES, MIP-1alpha or MCP-1. CONCLUSIONS:H. pylori was capable of inducing IL-8 production by human neutrophils, but not C-C chemokines. Production of C-X-C dominant chemokine by neutrophils is consistent with the pathological characteristics of H. pylori-induced gastritis, where persistent neutrophil infiltration is present.