Induction of maturation and cytokine release of human dendritic cells by Helicobacter pylori
Induction of maturation and cytokine release of human dendritic cells by Helicobacter pylori
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DOI：
10.1128/iai.72.8.4416-4423.2004
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发表时间：
2004-08-01
影响因子：
3.1
通讯作者：
Schneider-Brachert, W
中科院分区：
文献类型：
--
作者：
Kranzer, K;Eckhardt, A;Schneider-Brachert, W
幽门螺杆菌会导致人体胃部持续感染，从而导致慢性胃炎和消化性溃疡病。尽管有强烈的促炎症反应，但免疫系统无法清除微生物。然而，这种常见细菌的免疫逃逸机制尚不清楚。我们研究了幽门螺杆菌和人类树突状细胞之间的相互作用。树突状细胞 (DC) 是有效的抗原呈递细胞，也是先天性免疫系统和获得性免疫系统之间的重要介质。用不同浓度的幽门螺杆菌刺激 DC 8、24、48 和 72 小时，会导致剂量依赖性白细胞介素 6 (IL-6)、IL-8、IL-10 和 IL-12 的产生。来自大肠杆菌的脂多糖（LPS）是一种已知的 DC 成熟剂，被用作阳性对照。 LPS 刺激后的细胞因子释放与 H. pylori 诱导的细胞因子释放相当，但 IL-12 除外。与幽门螺杆菌诱导的大量 IL-12 相比，LPS 刺激后 IL-12 仅适度释放。我们进一步研究了幽门螺杆菌诱导 DC 成熟的潜力。对细胞表面成熟标记分子（例如 CD80、CD83、CD86 和 HLA-DR）表达的荧光激活细胞分选分析显示，在幽门螺杆菌或 LPS 刺激后，细胞表面表达有相同的上调。我们发现幽门螺旋杆菌血清阳性和血清阴性供体之间在细胞因子释放和表面分子上调方面没有显着差异。这些数据清楚地表明幽门螺杆菌诱导人类未成熟树突状细胞的强烈激活和成熟。
Helicobacter pylori causes a persistent infection in the human stomach, which can result in chronic gastritis and peptic ulcer disease. Despite an intensive proinflammatory response, the immune system is not able to clear the organism. However, the immune escape mechanisms of this common bacterium are not well understood. We investigated the interaction between H. pylori and human dendritic cells. Dendritic cells (DCs) are potent antigen-presenting cells and important mediators between the innate and acquired immune system. Stimulation of DCs with different concentrations of H. pylori for 8, 24, 48, and 72 h resulted in dose-dependent interleukin-6 (IL-6), IL-8, IL-10 and IL-12 production. Lipopolysaccharide (LPS) from Escherichia coli, a known DC maturation agent, was used as a positive control. The cytokine release after stimulation with LPS was comparable to that induced by H. pylori except for IL-12. After LPS stimulation IL-12 was only moderately released compared to the large amounts of IL-12 induced by H. pylori. We further investigated the potential of H. pylori to induce maturation of DCs. Fluorescence-activated cell sorting analysis of cell surface expression of maturation marker molecules such as CD80, CD83, CD86, and HLA-DR revealed equal upregulation after stimulation with H. pylori or LPS. We found no significant differences between H. pylori seropositive and seronegative donors of DCs with regard to cytokine release and upregulation of surface molecules. These data clearly demonstrate that H. pylori induces a strong activation and maturation of human immature DCs.