Xue Jia, Fan Xiaoxu, Yu Jing, Zhang Shouping, Xiao Jin, Hu Yanxin, Wang Ming
Key Laboratory of Animal Epidemiology and Zoonosis of Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University Beijing, China.
Key Laboratory of Animal Epidemiology and Zoonosis of Ministry of Agriculture, College of Veterinary Medicine, China Agricultural UniversityBeijing, China; China Animal Health and Epidemiology CenterQingdao, China.
Front Microbiol. 2016 Jun 15;7:924. doi: 10.3389/fmicb.2016.00924. eCollection 2016.
Highly pathogenic avian influenza virus (HPAIV) H5N1 is a highly contagious virus that can cause acute respiratory infections and high human fatality ratio due to excessive inflammatory response. Short-term heat shock, as a stressful condition, could induce the expression of heat shock proteins that function as molecular chaperones to protect cells against multiple stresses. However, the protective effect of short-term heat shock in influenza infection is far from being understood. In this study, mice were treated at 39°C for 4 h before being infected with HPAIV H5N1. Interestingly, short-term heat shock significantly increased the levels of HSP70 and pro-inflammatory cytokines IL-6, TNF-α, IFN-β, and IFN-γ in the lung tissues of mice. Following HPAIV H5N1 infection, short-term heat shock alleviated immunopathology and viral replication in lung tissue and repressed the weight loss and increased the survival rate of H5N1-infected mice. Our data reported that short-term heat shock provided beneficial anti-HPAIV H5N1 properties in mice model, which offers an alternative strategy for non-drug prevention for influenza infection.
高致病性禽流感病毒(HPAIV)H5N1是一种高传染性病毒,可引发急性呼吸道感染,并因过度炎症反应导致人类高死亡率。短期热休克作为一种应激条件,可诱导热休克蛋白的表达,这些蛋白作为分子伴侣发挥作用,保护细胞免受多种应激。然而,短期热休克在流感感染中的保护作用仍远未被了解。在本研究中,小鼠在感染HPAIV H5N1之前于39°C处理4小时。有趣的是,短期热休克显著提高了小鼠肺组织中HSP70和促炎细胞因子IL-6、TNF-α、IFN-β和IFN-γ的水平。在感染HPAIV H5N1后,短期热休克减轻了肺组织中的免疫病理学和病毒复制,并抑制了体重减轻,提高了H5N1感染小鼠的存活率。我们的数据表明,短期热休克在小鼠模型中具有有益的抗HPAIV H5N1特性,这为流感感染的非药物预防提供了一种替代策略。