Transcriptional mechanisms of acute lung injury

被引:205
|
作者
Fan, J [1 ]
Ye, RD [1 ]
Malik, AB [1 ]
机构
[1] Univ Illinois, Coll Med, Dept Pharmacol, Chicago, IL 60612 USA
关键词
nuclear factor-kappa B; transcription factor; cytokine; pulmonary inflammation;
D O I
10.1152/ajplung.2001.281.5.L1037
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Acute lung injury occurs as a result of a cascade of cellular events initiated by either infectious or noninfectious inflammatory stimuli. An elevated level of proinflammatory mediators combined with a decreased expression of anti-inflammatory molecules is a critical component of lung inflammation. Expression of proinflammatory genes is regulated by transcriptional mechanisms. Nuclear factor-kappaB (NF-kappaB) is one critical transcription factor required for maximal expression of many cytokines involved in the pathogenesis of acute lung injury. Activation and regulation of NF-kappaB are tightly controlled by a complicated signaling cascade. In acute lung injury caused by infection of bacteria, Toll-like receptors play a central role in initiating the innate immune system and activating NF-kappaB. Anti-inflammatory cytokines such as interleukin-10 and interleukin-13 have been shown to suppress inflammatory processes through inhibiting NF-kappaB activation. NF-kappaB can interact with other transcription factors, and these interactions thereby lead to greater transcriptional selectivity. Modification of transcription is likely to be a logical therapeutic target for acute lung injury.
引用
收藏
页码:L1037 / L1050
页数:14
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