Several factors have been shown to trigger the mechanisms for the pathologenesis of asthma and airway inflammation. Elevated levels of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the bronchoalveolar lavage fluid have been detected in asthmatic patients. Cytokines exert as potent stimuli in inflammatory responses through up-regulation of many gene expressions, including cytokines, chemokines, proteases, cyclooxygenase, and adhesion molecules. The extents of these gene expressions are correlated with the severity of inflammation. However, the intracellular signaling mechanisms underlying the expression of target proteins regulated by these factors are elusive.

The mechanisms underlying actions by cytokines may be integrated to the signaling networks that augment airway inflammation by recruiting leukocytes and lead to airway remodeling. Although cytokines have been reported to activate mitogen-activated protein kinases (MAPKs) including p42/p44 MAPK, p38, and c-jun-N-terminal kinase (JNK), the relationship between the activation of these pathways and expression of inflammatory genes remains unknown. Moreover, many genes regulated by MAPKs are dependent on NF-ĸB for transcription. NF-ĸB has also been shown to involve in target protein expression at the transcriptional level in various cell types. Therefore, this presentation will focus to review the mechanisms underlying the intracellular signalings involved in several target protein expression induced by cytokines  in airway resident cells. Increased understanding of signal transduction mechanisms underlying target protein gene regulation will create opportunities for the development of anti-inflammation, anti-cancer, and anti-metastasis therapeutic strategies.