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I mmunologically mediated inflammation undoubtedly plays a central role in the airway inflammation characteristic of asthma but such inflammation alone does not explain many of the characteristic pathological features of asthma. There is increasing evidence that the epithelium of the asthmatic airways is structurally and functionally abnormal and critically contributes to the inflammatory response and re-modeling of asthmatic airways. In asthmatics the airway epithelium secretes a variety of cytokines, chemokines and growth factors (e.g., PGE2, IL-8, IL-1, IL-6 eotaxin, RANTES, TNF-α, GM-CSF, TGFα/β) with increased responses to pathogenic and environmental stresses (e.g., air pollution, viral infection, oxidative stress) compared to healthy subjects. We have a program of work that is examining the effect of a number of environmental agents (house dust mite antigen, side stream tobacco smoke, nanoparticles) on the secretory function of cultured airway epithelial cells from neonates, children and adults with or without asthma. We are also examining the modulating effects of established asthma therapy such as the leukotriene antagonist Montelukast. This presentation will cover the background to our studies and present data on our key findings to date
https://www.omicsonline.org/2155-9899/2155-9899.S1.017-006.pdf