Syk-kinase inhibition prevents mast cell activation in nasal polyps.

摘要: BACKGROUND Mast cells are crucial effector in the allergic cascade. The cross-linking of high affinity IgE receptor (FceRI) activates mast and basophils. Spleen tyrosine kinase (Syk) is positioned upstream signal transducing pathway may represent an important target for treatment nasal inflammatory diseases. OBJECTIVE We measured effects a specific Syk inhibitor release cell mediators human cord blood-derived (CBDMCs) (in-vitro) tissue (ex-vivo). METHODS Surgical samples were collected from patients with polyposis who underwent sinus surgery. Tissue cubes +- 0.9 mm3 primed myeloma (1 microg/ml), preincubated NVP-QAB205 different concentrations then stimulated culture medium, anti-IgE 10 microg/ml 30 microg/ml. Supernatants analysed histamine, LTC4/LTD4/LTE4 PGD2. CBDMCs likewise pre-incubated compound, prior to stimulation at RESULTS In CBDMCs, prevented degranulation assessed by measurement histamine production Furthermore, was similarly able significantly inhibit these granules newly synthesized polyp dose dependent manner. CONCLUSION Although critical role transduction has been well documented vitro, this study supports importance receptor-mediated ex-vivo within tissue. Thus, inhibition therapeutic strategy upper airway disease involvement, such as rhinitis.