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Among constitutively present cells, bronchoactive leukotrienes are produced predominantly by mast cells1 and macrophages.2 A unique characteristic of asthmatic inflammation is the migration of leukocytes from the peripheral blood to the conducting airways of the lung. This is especially true of the eosinophil, which is not present in the airways of normal individuals, but may be found in massive numbers during periods of airway hyperresponsiveness in asthmatic individuals (fig1).3-5 Most experimental models indicate that eosinophils are an invariable component of asthmatic hyperresponsiveness, although some studies suggest that bronchoconstriction can occur in the relative absence of these cells.
For the purposes of this discussion, the eosinophil will be viewed as a leukotriene transport system capable of providing a substantial reservoir of bronchoactive leukotrienes to airways in relatively short time. They may be delivered to conducting airways in large numbers and have the capacity to produce cysteinyl leukotrienes (LTC4) which cannot be produced by neutrophils, but also migrate into conducting airways in some circumstances.6 7 This discussion …
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