Pneumonia is one important cause of mortality in neonates. However, the mechanism remains still unclear. Viral infection greatly enhances the morbidity of Streptococcus pneumonia. In this study, we tried to understand how human rhinovirus (HRV) would accelerate Streptococcus pneumonia infection. Alveolar macrophages (AMs) were isolated from neonatal mice. Cytokine concentrations were detected using ELISA. The phagocytosis of Streptococcus pneumonia by AMs was indicated by immunofluorescence. Toll-like receptor 3 (TLR3) and CD68 expression in isolated AMs or infected mice were determined by western blot or immunochemistry. The mortality was explored using Kaplan-Meier analysis. HRV infection enhanced cytokine release by AMs, and decreased Streptococcus pneumonia-induced TNF-α, IL-1β and IL-6 release by AMs, while has no influence on IL-10 release. HRV infection impaired phagocytosis of Streptococcus pneumonia in AMs. Mechanically, HRV infection up-regulated TLR3 expression in AMs. Mortality and pneumococcal burden decreased in TLR3-/- neonatal mice and inflammation and phagocytosis were restored in TLR3-/- AMs. Neonatal rhinovirus impairs the immune response of alveolar macrophages to facilitate Streptococcus pneumonia infection via TLR3 signaling.

中文翻译：

---

鼻病毒损害肺泡巨噬细胞的免疫反应，以促进肺炎链球菌感染。

肺炎是新生儿死亡的重要原因之一。但是，机制仍不清楚。病毒感染大大增加了链球菌肺炎的发病率。在这项研究中，我们试图了解人类鼻病毒（HRV）如何加速链球菌肺炎的感染。从新生小鼠中分离出肺泡巨噬细胞（AMs）。使用ELISA检测细胞因子浓度。通过免疫荧光指示AMs对肺炎链球菌的吞噬作用。通过蛋白质印迹或免疫化学测定分离的AM或感染的小鼠中的Toll样受体3（TLR3）和CD68表达。使用Kaplan-Meier分析探索死亡率。HRV感染增强AMs释放细胞因子，并降低AMs释放链球菌肺炎诱导的TNF-α，IL-1β和IL-6，而对IL-10释放没有影响。HRV感染会损害AMs中链球菌肺炎的吞噬作用。在机械上，HRV感染上调了AMs中TLR3的表达。TLR3-/-新生小鼠的死亡率和肺炎球菌负担降低，TLR3-/-AMs的炎症和吞噬作用得以恢复。新生儿鼻病毒会削弱肺泡巨噬细胞的免疫反应，从而通过TLR3信号传导促进肺炎链球菌感染。