Chicken IL‐6 is a heat‐shock gene
Chicken IL‐6 is a heat‐shock gene
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DOI：
10.1016/j.febslet.2013.09.012
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发表时间：
2013-11
期刊：
影响因子：
3.5
通讯作者：
R. Prakasam;M. Fujimoto;Ryosuke Takii;Naoki Hayashida;E. Takaki;K. Tan;Fangxu Wu;S. Inouye;A. Nakai
中科院分区：
文献类型：
--
作者：
R. Prakasam;M. Fujimoto;Ryosuke Takii;Naoki Hayashida;E. Takaki;K. Tan;Fangxu Wu;S. Inouye;A. Nakai
发热反应是由致热细胞因子引起的，包括响应于脊椎动物中的微生物感染和疾病的IL-6。哺乳动物HSF 1可感知温度升高，通过抑制致热细胞因子表达来负调节反应。我们发现，HSF 3，一种禽类HSF 1的直系同源物，在鸡细胞热休克过程中直接结合并激活sIL-6。发热反应机制的其他组分，如IL-1β和ATF 3，在哺乳动物和鸡细胞中也受到不同的调节。这些结果表明，在鸟类中，由HSF 3-IL-6通路组成的前馈回路加剧了发热反应。
The febrile response is elicited by pyrogenic cytokines including IL-6 in response to microorganism infections and diseases in vertebrates. Mammalian HSF1, which senses elevations in temperature, negatively regulates the response by suppressing pyrogenic cytokine expression. We here showed that HSF3, an avian ortholog of mammalian HSF1, directly binds to and activatesIL-6during heat shock in chicken cells. Other components of the febrile response mechanism, such as IL-1β and ATF3, were also differently regulated in mammalian and chicken cells. These results suggest that the febrile response is exacerbated by a feed-forward circuit composed of the HSF3-IL-6 pathway in birds.