作者: Ruxana T Sadikot , Heng Zeng , Fiona E Yull , Bo Li , Dong-sheng Cheng
DOI: 10.4049/JIMMUNOL.172.3.1801
关键词:
摘要: We examined the role of redox signaling generated by NADPH oxidase in activation NF-kappaB and host defense against Pseudomonas aeruginosa pneumonia. Using mice with an NF-kappaB-driven luciferase reporter construct (HIV-LTR/luciferase (HLL)), we found that intratracheal administration P. resulted a dose-dependent neutrophilic influx NF-kappaB. To determine effects reactive oxygen species system on NF-kappaB, crossbred deficient p47(phox) (p47(phox-/-)HLL). These p47(phox-/-)HLL were unable to activate same degree as HLL intact following infection. In addition, lung TNF-alpha levels significantly lower compared mice. Bacterial clearance was impaired vitro studies using bone marrow-derived macrophages showed Toll-like receptor 4 necessary for treatment aeruginosa. Additional from p47(phox-/-) confirmed maximal 4-dependent this model. data indicate oxidase-dependent respiratory burst stimulated infection contributes modulating redox-dependent through pathway.