**1. Introduction**

Nuclear factor-κB (NF-κB) is a nuclear transcription factor first recognized in 1986 by Sen and Baltimore. Its name derives from the fact that it was first diagnosed in the nuclei of B cells [1- 3] bound to an enhancer element of the immunoglobulin kappa light chain gene [4]. At that time, NF-κB was primarily thought to be a B-cell–specific transcription factor, but it was afterward found to be present in every cell type [5]. NF-κB has been implicated in the regulation of host inflammatory [6-8] and immune responses [9-11], cell adhesion [12], developmental signals [13], cell proliferation, differentiation [14, 15] and in defending cells from apoptosis [16, 17]. In addition, it plays important roles in cellular growth properties by encoding cytokines, chemokines and receptors required for neutrophil adhesion and migration, thus increasing the expression of specific cellular genes [18].

Physical and chemical damage to the lung causes an inflammatory response, thus defending the lung against the causative agents. Inflammation initiates a series of cellular procedures which lead to healing the injury; however, if resolving the inflammatory response is inefficient, the result is a chronic situation. Numerous pathophysiologic conditions and inhaled air pollutants are identified as generating stable stimulation of phagocytic cells, leading to the amplification of proinflammatory cytokines, and mediating chronic inflammation in the lung [19].

Many studies have reported the role of NF-kB in inflammation and proven the association of NF-κB with human inflammatory lung diseases. The point of this short review is to summarize what is known about the molecular biology and activation pathway of NF-κB and to highlight the role of NF-κB in the pathogenesis of inflammatory lung disease, as well as in asthma, COPD, ARDS, and cystic fibrosis.
