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Modulation of Innate Cytokine Responses by Products of Helicobacter pylori

机译：幽门螺杆菌产物对天然细胞因子应答的调节

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The gastric inflammatory and immune response in Helicobacter pylori infection may be due to the effect of different H. pylori products on innate immune mechanisms. The aim of this study was to determine whether bacterial components could modulate cytokine production in vitro and thus contribute to Th1 polarization of the gastric immune response observed in vivo. The effect of H. pylori recombinant urease, bacterial lysate, intact bacteria, and bacterial DNA on proliferation and cytokine production by peripheral blood mononuclear cells (PBMCs) from H. pylori-negative donors was examined as a model for innate cytokine responses. Each of the different H. pylori preparations induced gamma interferon (IFN-γ) and interleukin-12p40 (IL-12p40), but not IL-2 or IL-5, production, and all but H. pylori DNA stimulated release of IL-10. Addition of anti-IL-12 antibody to cultures partially inhibited IFN-γ production. In addition, each bacterial product inhibited mitogen-stimulated IL-2 production by PBMCs and Jurkat T cells. The inhibitory effect of bacterial products on IL-2 production correlated with inhibition of mitogen-stimulated lymphocyte proliferation, although urease inhibited IL-2 production without inhibiting proliferation, suggesting that inhibition of IL-2 production alone is not sufficient to inhibit lymphocyte proliferation. The results of these studies demonstrate that Th1 polarization of the gastric immune response may be due in part to the direct effects of multiple different H. pylori components that enhance IFN-γ and IL-12 production while inhibiting both IL-2 production and cell proliferation that may be necessary for Th2 responses.
机译：幽门螺杆菌感染中的胃炎和免疫反应可能是由于不同的 H作用所致。幽门螺杆菌产物对先天免疫机制的影响。这项研究的目的是确定细菌成分是否可以在体外调节细胞因子的产生，从而促进体内观察到的胃免疫反应的Th1极化。 H的影响。幽门螺杆菌重组脲酶，细菌裂解物，完整细菌和细菌DNA对 H外周血单个核细胞（PBMC）增殖和细胞因子产生的影响。将幽门螺杆菌阴性供体作为先天细胞因子反应的模型。每个不同的 H。幽门螺杆菌制剂诱导γ-干扰素（IFN-γ）和白介素12p40（IL-12p40），但不诱导IL-2或IL-5的产生，除了 H。幽门螺杆菌DNA刺激了IL-10的释放。向培养物中添加抗IL-12抗体可部分抑制IFN-γ的产生。此外，每种细菌产物均抑制PBMC和Jurkat T细胞通过促分裂原刺激的IL-2产生。细菌产物对IL-2产生的抑制作用与抑制有丝分裂原刺激的淋巴细胞的增殖有关，尽管脲酶可抑制IL-2的产生而不抑制增殖，这表明仅抑制IL-2的产生不足以抑制淋巴细胞的增殖。这些研究的结果表明，胃免疫反应的Th1极化可能部分归因于多种不同的 H的直接作用。幽门螺杆菌成分，可增强IFN-γ和IL-12的产生，同时抑制IL-2的产生和细胞增殖，这可能是Th2反应所必需的。

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