Mast cells are an exceptionally rich source of prostaglandins D2 (PGD2). PGD2 is pro-inflammatory and, together with other mast cell-derived mediators such as histamine and cysteinyl-leukotrienes (cys-LTs), can cause bronchoconstriction. The enzyme cyclooxygenase (COX) is central to the generation of prostanoids such as PGD2. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit COX. COX exists as two isoforms, COX-1 and COX-2. Mediator release experiments using human lung mast cells were performed with mouse anti-IgE. These cells express endogenous IgE, so they are responsive to anti-IgE without the need for passive sensitization with exogenously added IgE. The histamine released in the supernatants of these cells is derived from degranulation, while prostaglandins and leukotrienes are derived from de novo synthesis.
A random selection of NSAIDs (aspirin, naproxen, ibuprofen, and diclofenac) was incubated with mast cells for 15 minutes without any additional stimuli. The effects of these NSAIDs on mediator release were evaluated. The figure above shows the results of this evaluation.