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Department of Pharmacology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612
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-
B (NF-B) 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-B 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-B. Anti-inflammatory cytokines such as interleukin-10 and interleukin-13 have been shown to
suppress inflammatory processes through inhibiting NF-B activation.
NF-B 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.
nuclear factor-B; transcription factor; cytokine; pulmonary
inflammation
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