Essential role of IL-6 in protection against H1N1 influenza virus by promoting neutrophil survival in the lung.
Essential role of IL-6 in protection against H1N1 influenza virus by promoting neutrophil survival in the lung.
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流感病毒感染被认为是全球主要的公共卫生问题。最常见流感病毒株（例如 H1N1）的季节性感染通常可以得到解决，但仍然会导致很高的死亡率。影响感染结果的因素仍不清楚。在这里，我们表明，IL-6 或 IL-6 受体的缺陷足以使正常亚致死剂量的 H1N1 甲型流感病毒导致小鼠死亡。 IL-6 通过保护中性粒细胞免受病毒引起的肺部死亡并促进中性粒细胞介导的病毒清除，对于解决流感感染是必需的。 IL-6 的缺失会导致流感病毒在肺部持续存在，从而导致明显的肺部损伤，并最终导致死亡。因此，我们证明 IL-6 是一种重要的先天免疫细胞因子，可以提供针对甲型流感感染的保护。损害 IL-6 产生或信号传导的遗传或环境因素可能会增加流感病毒感染的死亡率。
Influenza virus infection is considered a major worldwide public health problem. Seasonal infections with the most common influenza virus strains (e.g. H1N1) can usually be resolved, but they still cause a high rate of mortality. The factors that influence the outcome of the infection remain unclear. Here we show that deficiency of IL-6 or IL-6 receptor is sufficient for normally sublethal doses of H1N1 influenza A virus to cause death in mice. IL-6 is necessary for the resolution of influenza infection by protecting neutrophils from virus-induced death in the lung and by promoting neutrophil-mediated viral clearance. Loss of IL-6 results in persistence of influenza virus in the lung leading to pronounced lung damage and, ultimately, death. Thus, we demonstrate that IL-6 is a vital innate immune cytokine in providing protection against influenza A infection. Genetic or environmental factors that impair IL-6 production or signalling could increase mortality to influenza virus infection.