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Helicobacter pylori induces dendritic cell maturation and th1 cytokine production

Helicobacter pylori induces dendritic cell maturation and th1 cytokine production

Digestive Disease Week Abstracts & Itinerary Planner : Abstract No W910

Background: Helicobacter pylori (HP) is an extracelluar organism that resides in the mucous layer of the gastric epithelium. Evidence suggests that HP can induce gastric inflammation without invading mucosal cells. It is believed that HP binds to gastric epithelial cells and stimulates the secretion of inflammatory cytokines. Breakdown of the epithelial barrier ensues allowing translocation of HP bacterial antigens which further stimulates antigen presenting cells (APC), e.g., macrophages in the l amina propria. However, it is known that tissue dendritic cells are a more efficient APC. A recent study by Rescigno et al. reported the ability of intestinal dendritic cells (DCs) to sample the lumen for the presence of bacteria without disturbing the i ntegrity of the epithelial barrier (Nature Medicine 2:361, 2001). It is unclear whether a similar process can occur in the stomach and thus whether HP triggers its Th1 immune response by activating dendritic cells. Aims: The goal of this study was to d et ermine whether live HP can induce DC maturation and Th1 cytokine release. Methods: Seven-day old bone marrow-derived DCs were obtained from C57BL/6 mice and were co-cultured with PBS or 108 organisms/ml of actively proliferating HP for 24 h. D Cs co-cultured with PBS served as controls. DCs were dual-labeled with FITC-MHC II and PE-CD40, PE-IL-12 or PE-IL-10 and analyzed by FACS. CD40 is a surface antigen expressed on mature dendritic cells involved in T cell activation. The mean for two exp eriments performed in triplicate are shown +/- the range. Results: Surface staining revealed that HP induced a two-fold increase in the percent of DCs expressing CD40 (PBS=16.9 +/- 8.7% , HP=35.4 +/- 4.6%). Intracellular cytokine staining showed a signif icantly higher percent of DCs expressing IL-12 (PBS=2 +/- 0.06%, HP=26.1 +/- 0.4%). No significant difference was seen for IL-10 (PBS 1.5 +/- 0.13%, HP=2.8 +/- 0.45%). Conclusions: HP induces DC maturation and Th1 cytokine release. These findings implicate a potential role of DCs as the APC mediating HP-induced gastritis.

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Accession: 035021558

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DOI: 10.1016/S0016-5085(03)83001-9

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