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Mast-cell activation mediated by the high-affinity receptor for IgE (FcepsilonRI) is considered to be a key event in the allergic inflammatory response. However, in a physiological setting, other receptors, such as KIT, might also markedly influence the release of mediators by mast cells. Recent studies have provided evidence that FcepsilonRI-dependent(More)
The mast cell is a central player in allergy and asthma. Activation of these cells induces the release of preformed inflammatory mediators localized in specialized granules and the de novo synthesis and secretion of cytokines, chemokines, and eicosanoids. The balance of engaging inhibitory and activatory cell-surface receptors on mast cells determines(More)
Mast cell mediator release represents a pivotal event in the initiation of inflammatory reactions associated with allergic disorders. These responses follow antigen-mediated aggregation of immunoglobulin E (IgE)-occupied high-affinity receptors for IgE (Fc epsilon RI) on the mast cell surface, a response which can be further enhanced following stem cell(More)
We have developed an improved thin-layer chromatographic method for separation of lung phospholipids. Individual phospholipids are completely separated in the first dimension. All phospholipids, except phosphatidylcholine, are then removed. The phosphatidylcholine-containing area is reacted with osmium tetroxide and saturated phosphatidylcholine species are(More)
Degranulation of mast cells in response to Ag or the calcium mobilizing agent, thapsigargin, is dependent on emptying of intracellular stores of Ca(2+) and the ensuing influx of external Ca(2+), also referred to as store-operated calcium entry. However, it is unlikely that the calcium release-activated calcium channel is the sole mechanism for the entry of(More)
Our previous studies demonstrated that propranolol, an inhibitor of phosphatidic acid phosphohydrolase (PAPase) (EC 3.1.3.4) blocks the IgE-dependent mediator release from a rat mast (RBL 2H3) cell line. To continue these studies, we examined the ability of propranolol to inhibit the IgE-dependent or ionomycin-mediated phosphoinositide hydrolysis and(More)
In recent years, the field of mast cell biology has expanded well beyond the boundaries of atopic disorders and anaphy laxis, on which it has been historically focused. The biochemical and signaling events responsible for the development and regulation of mast cells has been increasingly studied, aided in large part by novel breakthroughs in laboratory(More)
By releasing multiple pro-inflammatory mediators upon activation, mast cells are critical effector cells in the pathogenesis of allergic inflammation. The traditional viewpoint of antigen-dependent mast cell activation is that of a Th(2)-driven process whereby antigen-specific IgE molecules are produced by B cells followed by binding of the IgE to high(More)
Although primarily required for the growth, differentiation, and survival of mast cells, Kit ligand (stem cell factor) is also required for optimal antigen-mediated mast cell activation. Therefore, concurrent inhibition of Kit- and FcepsilonRI-mediated signaling would be an attractive approach for targeting mast cell-driven allergic reactions. To explore(More)
We examined the effect of purinoceptor agonists on phosphatidylcholine secretion in primary cultures of type II pneumocytes from adult rats. Surfactant is a major product of the type II cell and phosphatidylcholine is its principal component. Adenosine, AMP, ADP and ATP stimulated phosphatidylcholine secretion in a concentration-dependent manner. At the(More)