Respiratory tract infections are a global health problem. The main causative agents of these infections are influenza A virus (IAV), Staphylococcus aureus (S. aureus), and Streptococcus pneumoniae (S. pneumoniae). Major research focuses on genetics and immune responses in these infections. Eicosanoids and other oxylipins are host-derived lipid mediators that play an important role in the activation and resolution of inflammation. In this study, we assess, for the first time, the different intracellular profiles of these bioactive lipid mediators during S. aureus LUG2012, S. pneumoniae TIGR4, IAV, and corresponding viral and bacterial co-infections of 16HBE cells. We observed a multitude of altered lipid mediators. Changes in the amount of 5-hydroxyeicosatetraenoic acid (5-HETE) were prominent for all bacterial infections. The infection with S. pneumoniae showed the strongest impact on bioactive lipid production and led to alterations in the amount of PPARγ ligands and precursors of pro-resolving lipid mediators.

中文翻译：

---

16HBE细胞脂质介体对呼吸道病原体单株和合并感染的反应

呼吸道感染是全球性的健康问题。这些感染的主要病原体是甲型流感病毒（IAV），金黄色葡萄球菌（S. aureus）和肺炎链球菌（S. pneumoniae）。重大研究集中于这些感染的遗传学和免疫反应。类花生酸和其他脂蛋白是宿主衍生的脂质介体，在炎症的激活和消退中起重要作用。在这项研究中，我们首次评估了在金黄色葡萄球菌LUG2012，肺炎链球菌感染期间这些生物活性脂质介体的不同细胞内特征。TIGR4，IAV以及16HBE细胞的相应病毒和细菌共感染。我们观察到大量改变的脂质介体。在所有细菌感染中，5-羟基二十碳四烯酸（5-HETE）的量变化都很明显。肺炎链球菌感染对生物活性脂质产生影响最大，并导致PPARγ配体和亲分解脂质介体前体的数量发生改变。