IL-1β expression is increased in response to P. aeruginosa infection, but the responsible proteins have not been clearly elucidated. Here, we demonstrate for the first time that IL-1β expression is induced in response to the heat shock protein 70-like protein DnaK. Treatment with recombinant DnaK (rDnaK) increased IL-1β expression in a dose- and time-dependent manner, and the release of mature IL-1β in response to rDnaK was detected to an extent similar to that stimulated by the well-known agonists, lipopolysaccharide and nigericin. rDnaK-mediated IL-1β expression was driven by the NF-κB signaling pathway. In addition, expression was controlled by the JNK signaling pathway, although these two signaling cascades act independently upon rDnaK stimulation. Finally, rDnaK-induced IL-1β expression was initiated via the action of TLR4. Taken together, the data reveal that P. aeruginosa-derived DnaK induces expression of IL-1β via TLR4-dependent activation of the NF-κB and JNK signaling pathways.

中文翻译：

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铜绿假单胞菌HSP70样蛋白DnaK通过TLR4依赖性激活NF-κB和JNK信号通路诱导IL-1β表达。

响应于铜绿假单胞菌感染，IL-1β表达增加，但尚未明确阐明其负责蛋白。在这里，我们首次证明响应热休克蛋白70样蛋白DnaK诱导IL-1β表达。重组DnaK（rDnaK）的处理以剂量和时间依赖性方式增加IL-1β的表达，并且检测到对rDnaK响应的成熟IL-1β的释放程度与众所周知的激动剂所刺激的程度相似，脂多糖和尼日利亚。rDnaK介导的IL-1β表达是由NF-κB信号通路驱动的。另外，尽管这两个信号级联在rDnaK刺激上独立起作用，但表达受JNK信号通路控制。最后，rDnaK诱导的IL-1β表达是通过TLR4的作用启动的。在一起