The epigeneticanalysis of secondary bacterial pneumonia following influenza virus infection

流感病毒感染的主要死亡原因是继发性细菌性肺炎。SET结构域分叉2（SETDB 2）是一种导致基因抑制的酶，其表达在巨噬细胞和支气管上皮细胞中增加，随后是I型干扰素（一种对抗病毒感染的必需细胞因子）和流感病毒刺激本身。SETDB 2的表达依赖于I型干扰素（IFN-I），在继发性细菌感染模型中，IFN-I受体敲除小鼠的存活率明显高于野生型小鼠。这些结果表明，SETDB 2有可能成为预防流感病毒感染后继发性细菌性肺炎的临床关键。

The main cause of death in influenza viral infection is secondary bacterial pneumonia. The expression of SET domain bifurcated 2 (SETDB2), an enzyme which leads to gene depression, was increased in both macrophages and bronchial epithelial cells, followed bytype-I interferon (an essential cytokine against viral infection) and influenza viral stimulation itself. The expression of SETDB2is type-I interferon (IFN-I) dependent, and IFN-I receptor knockout mice improved a significant survival compared with wild-type mice in secondary bacterial infectious model. There results suggest that SETDB2 has the potential to be a clinical key to prevent secondary bacterial pneumonia following influenza viral infection.