Increasing evidence has suggested mat airway epithelium plays an essential role in the modulation of airway innate and adaptive immune responses in addition to serving as a physical barrier against microbial infection and exterior insults. The nature of this modulation and the potential mediators involved are currently unresolved. Interleukin (IL)-17A recently emerged as a potential candidate for directly modulating innate and adaptive iiunune responses. Our laboratory has recently shown that IL-17A is one of the most potent cytokines among a panel of 21 cytokines (IL-1α, 1β, 2,3,4,5,6,7,8,9,10,11,12,13, 15, 16, 18, IFN-γ, GM-CSF, and TNF-α) to stimulate the expression of β- defensin 2 (HBD-2) and CCL-20 (MIP-3) by primary human airway epithelial cells (Kao et al., J. of Immunol. 173: 3482-3491, 2004; Kao et al., J. of Immunol. 175: 6676-6685, 2005). Through Afrymetrix genechips and quantitative-PCR, we identified the following IL-17A-induced genes in well-differentiated normal human bronchial epithelium (NHBE):IL-19; GRO-α,-β,-γ; CXC-5 and GCP-2, in addition to known inducible cytokines, CCL20, IL-8, and HBD2. Since (he elevated presence of IL-17A has been demonstrated in a variety of airway diseases including those related to microbial infection, COPD, and Th2-dominated diseases, the induction of these diverse cytokines may further support the critical role of IL-17A in the pathogenesis of airway diseases and airway inflammation.Airway remodeling and persistent inflammation are common features of various airway diseases, especially allergic asthma. Most of these events are regulated by a complex series of interplays between the surrounding cells/tissues and the cytokines/mediators that are present in the airway lumen and walls. Despite their complexity and prominent location hi airway anatomy, the epithelia are frequently treated as a passive target rather than an active participant in the modulation of the pathogenesis of disease. Increasingly it is believed that airway epithelia, rather than serving as a barrier function and a passive target of disease symptoms, are actively involved in the modulation of disease. The epithelia are important reservoirs for the production of various cytokines that regulate mucosal immunity and airway inflammation. Despite of this recognition, the nature of this modulation and the potential mediators involved are currently unresolved. Interleukin (IL)-17A recently emerged as a potential candidate for directly modulating innate and adaptive immune responses, especially in airways infected with bacteria (1).
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