Understanding of pathogenesis and protection mechanisms underlying influenza-Streptococcus pneumoniae co-infection may provide potential strategies for decreasing its high morbidity and mortality. Interleukin-6 (IL-6) is an important cytokine that acts to limit infection-related inflammation; however, its role in co-infected pneumonia remains unclear. Here we show that the clinically relevant co-infected mice displayed dramatically elevated IL-6 levels; which was also observed in patients with co-infected pneumonia. IL-6 -/- mice presented with increased bacterial burden, early dissemination of bacteria to extrapulmonary sites accompanied by aggravated pulmonary lesions and high mortality when co-infection. This protective function of IL-6 is associated with cellular death and macrophage function. Importantly, therapeutic administration of recombinant IL-6 protein reduced cells death in BALF, and enhanced macrophage phagocytosis through increased MARCO expression. This protective immune mechanism furthers our understanding of the potential impact of immune components during infection and provides potential therapeutic avenues for influenza-Streptococcus pneumoniae co-infected pneumonia.

中文翻译：

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流感-肺炎链球菌共感染肺炎A保护剂期间的IL-6。

了解流感-肺炎链球菌共感染的发病机理和保护机制可能为降低其高发病率和死亡率提供潜在策略。白细胞介素6（IL-6）是一种重要的细胞因子，可限制感染相关的炎症。然而，其在合并感染性肺炎中​​的作用仍不清楚。在这里，我们显示临床相关的共同感染小鼠表现出显着升高的IL-6水平。在合并感染的肺炎患者中也观察到这种情况。IL-6-/-小鼠的细菌负荷增加，细菌向肺外部位的早期传播，伴有严重的肺部病变，并且在合并感染时死亡率较高。IL-6的这种保护功能与细胞死亡和巨噬细胞功能有关。重要的，重组IL-6蛋白的治疗性给药减少了BALF中的细胞死亡，并通过增加了MARCO的表达增强了巨噬细胞的吞噬作用。这种保护性免疫机制使我们进一步了解了感染期间免疫成分的潜在影响，并为流感-肺炎链球菌共感染性肺炎提供了潜在的治疗途径。