“…Mast cells are one of the primary contributors to this via release of pre-formed histamine, tryptase, and chymase, as well as by producing cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-4, and IL-5. These mast cell products are responsible for increasing vascular permeability, Th2 lymphocyte development, and eosinophil attraction leading to bronchoconstriction; and the upregulation of a number of secondary inflammatory and chemotactic products including PGE 2 , IL-1β, TNF-α, IL-8, and regulation on activation, normal T cell-expressed and -secreted (RANTES). This study used a model developed in our laboratory (11,12) of in vitro FA manipulation in a respiratory cell line (A549) to examine the hypothesis that changes in membrane PUFA would significantly alter the production of inflammatory mediators in response to mediators of allergic disease. We examined the effect of manipulation of membrane phospholipid on the production of cytokines (IL-1β, TNF-α, IL-8, RANTES) and PGE 2 by respiratory epithelial cells in response to stimulation by mast cell mediators of allergic disease (histamine, TNF-α, IL-4, IL-5).…”