In addition, previous studies have been targeting on the effect of TGF-b signaling on epithelium apoptosis. However, our data demonstrate that there is no significant change in cell apoptosis Oroxin-B between the wild type and CC10-Smad7 transgenic mice, indicating that apoptosis may not play a primary role in TGFb-mediated regulation on airway inflammation. Our analyses with the cytokine profile in the lung homogenates provided additional evidence that TGF-b signaling in the epithelium itself is implicated in the development of allergic response. We found that the well-defined Th2 cytokines, such as IL-4, IL-5 and IL-13, were significantly decreased in the Smad7 transgenic mouse, indicating that the Th2-driven allergic inflammation is alleviated after disruption of TGF-b signaling in airway epithelium. It can be postulated that there exists a positive feedback between the activation of epithelial cells and the Th2 cells, and TGF-b signaling in epithelial cells is implicated in such positive feedback. Airway epithelial cells can Crocin-I undergo remodeling changes and contribute to inflammation by producing proinflammatory molecules. Indeed, epithelial cells can secrete an array of proinflammatory molecules that modulate the recruitment and functioning of immune and inflammatory cells. As cytokines play a critical role in orchestrating, perpetuating and amplifying the inflammatory response in asthma, we hypothesize that the secretion of proinflammatory cytokines, and/or the positive feedback between epithelial cells and Th2 cells, are partly controlled by TGF-b signaling in epithelial cells. In addition to Th2 cytokines, some other cytokines such as IL-1 and IL-6 that have been found to play a role in many inflammatory diseases, were also reduced in the Smad7 transgenic mice, indicating that TGF-b signaling in the airway epithelium has a general effect to modulate local inflammation. Interestingly, we found that IL-10 is increased in the lung homogenate of CC10Smad7 mice. Consistently, IL-10 has been shown to reduce both Th1- and Th2-driven inflammatory processes.