Our understanding of the specific factors controlling the onset, development and resolution of the acute inflammatory response has increased considerably in recent years. Requirements for specific cytokines, chemokines and adhesion molecules have been identified and the mechanisms by which these factors regulate neutorphil recruitment to site of inflammation has been determined. Current studies deal with defining the molecular mechanisms by which various stimuli initiate and propagate or downregulate the inflammatory response in lung. At the heart of these processes lies the nuclear factor-κB (NF-κB). A ubiquitous transcriptional activating factor, NF-κB regulates the expression of many proinflammatory cytokines, chemokines and adhesion molecules and represents a potential target for therapeutic intervention. In unstimulated cells, NF-κB is retained in the cytoplasm by inhibitory proteins of the IκB family. Upon cell activation, IκB proteins are degraded and NF-κB translocates to the nucleus where it binds to specific DNA sequences. Nuclear translocation, which defines activation of NF-κB, can be suppressed in lung by the anti-inflammatory cytokines, interlukin-10 and interleukin-13. This inhibitory process appears to be due to preservation of the inhibitory protein, IκBa. The present review discusses the role of NF-κB in acute inflammatory lung injury.