作者: Zheng Pang , Robert D. Junkins , Adam J. MacNeil , Craig McCormick , Zhenyu Cheng
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摘要: Infection with the opportunistic pathogen Pseudomonas aeruginosa is effectively controlled through tightly coordinated inflammation in healthy individuals. Dysregulated cystic fibrosis greatly increases susceptibility to P. and lung damage. Recently, we identified regulator of calcineurin-1, a small, conserved protein that suppresses NFAT pathway by inhibition calcineurin functions as central negative multiple inflammatory transcription factors after infection, implying role for canonical infection. Calcineurin calcium-calmodulin-responsive phosphatase dephosphorylates promotes nuclear translocation transcriptional activity. The contribution host defense against remains poorly characterized. In this study, found was rapidly transiently activated infection both vitro vivo. Deficiency Aβ caused impaired activation decreased cytokine production Finally, demonstrated cross-talk between NFкB pathways coordinately transactivate response genes during Together, these results demonstrate first time interacts contributes response.