Inducible Activation of TLR4 Confers Resistance to Hyperoxia-Induced Pulmonary Apoptosis
作者： Salman T. Qureshi , Xuchen Zhang , Erika Aberg , Nicolas Bousette , Adel Giaid
DOI: 10.4049/JIMMUNOL.176.8.4950
关键词:
摘要: TLRs are essential mediators of host defense against infection via recognition unique microbial structures. Recent observations indicate that TLR4, the principal receptor for bacterial LPS, may also be activated by noninfectious stimuli including host-derived molecules and environmental oxidant stress. In mice, susceptibility to ozone-induced lung permeability has been linked wild-type allele whereas deficiency TLR4 predisposes lethal injury in hyperoxia. To precisely characterize role epithelial expression response stress, we have created an inducible transgenic mouse model targets human signaling domain airways. Exposure induced mice hyperoxia revealed a significant reduction pulmonary apoptosis compared with controls. This phenotype was associated sustained up-regulation antiapoptotic such as heme oxygenase-1 Bcl-2, yet only transient activation transcription factor NF-κB. Specific vivo knockdown or Bcl-2 intranasal administration short interfering RNA blocked effect on hyperoxia-induced apoptosis. These results define novel modulator cellular
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