EPA competitively inhibits the formation of leukotrienes
from arachidonic acids and v-6 fatty acids and reduces
the generation of cytokines from inflammatory cells. It
has previously been found that EPA inhibits the immunoglobulin
E-induced release from cultured human mast
cells of prostaglandin D2 but not of histamine [16, 17].
Histamine is an important preformed mediator of immediate-
type hypersensitivity. The inability of EPA to
inhibit the release of histamine from mast cells may
explain why treatment with EPA blocked the late
response to inhaled allergens but not the immediate
response in patients with asthma.