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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Bacterial challenge stimulates formation of arachidonic acid metabolites by human keratinocytes and neutrophils in vitro.
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Bacterial challenge stimulates formation of arachidonic acid metabolites by human keratinocytes and neutrophils in vitro.

机译：细菌攻击在体外刺激人角质形成细胞和中性粒细胞形成花生四烯酸代谢物。

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Although the interactions of bacteria with keratinocytes induce the synthesis of various mediators, the capability of epithelial cells to form arachidonic acid mediators has not been studied, and therefore the first part of this study was initiated. The complex mixture of epithelium-derived mediators suggests that chemoattraction is not their only effect on neutrophils and that they may also affect neutrophil mediator synthesis. The effect of epithelium-derived mediators on neutrophil eicosanoide synthesis was evaluated in the second part of this study. We incubated human keratinocytes with human-pathogenic bacteria for 2 h and harvested the supernatants after 4, 6, 10, and 18 h of culture. Subsequently, the supernatants were coincubated for 5 min with human neutrophils with or without arachidonic acid. The formation of the arachidonic acid metabolites prostaglandin E(2) (PGE(2)), leukotriene B(4) (LTB(4)), 12-hydroxyeicosatetraenoic acid (12-HETE), and 15-HETE in keratinocytes and neutrophils was measured by reverse-phase high-pressure liquid chromatography. We demonstrated for the first time that keratinocytes produced significant amounts of LTB(4) and 12-HETE 4 to 6 h after bacterial challenge. Upon stimulation with epithelial supernatants, neutrophils produced significant amounts of PGE(2), LTB(4), 12-HETE, and 15-HETE throughout the observation period of 18 h, with a maximum synthesis by supernatants harvested 4 to 10 h after bacterial infection. The results of the study suggest that arachidonic acid mediator formation by epithelial cells following bacterial challenge may act as an early inflammatory signal for the initiation of the immune response. The epithelial supernatants were capable of inducing the formation of arachidonic acid mediators by neutrophils, which may have further regulatory effects on the immune response.
机译：尽管细菌与角质形成细胞的相互作用诱导各种介质的合成，但尚未研究上皮细胞形成花生四烯酸介质的能力，因此开始了本研究的第一部分。上皮衍生介质的复杂混合物表明，化学吸引并不是它们对中性粒细胞的唯一影响，它们也可能影响中性粒细胞介质的合成。本研究的第二部分评估了上皮衍生介质对中性粒细胞类花生酸合成的影响。我们将人角质形成细胞与人类致病菌一起孵育 2 小时，并在培养 4、6、10 和 18 小时后收获上清液。随后，将上清液与含或不含花生四烯酸的人中性粒细胞共同孵育 5 分钟。采用反相高压液相色谱法检测角质形成细胞和中性粒细胞中花生四烯酸代谢产物前列腺素E（2）（PGE（2））、白三烯B（4）（LTB（4））、12-羟基二十碳四烯酸（12-HETE）和15-HETE的形成。我们首次证明角质形成细胞在细菌攻击后 4 至 6 小时产生大量 LTB（4） 和 12-HET。在上皮上清液刺激下，中性粒细胞在18小时的观察期间产生大量的PGE（2），LTB（4），12-HETE和15-HETE的合成量最大，细菌感染后4至10小时收获的上清液合成量最大。研究结果表明，细菌攻击后上皮细胞形成的花生四烯酸介质可能作为免疫反应启动的早期炎症信号。上皮上清液能够诱导中性粒细胞形成花生四烯酸介质，这可能对免疫反应产生进一步的调节作用。

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