Suppression by ingested eicosapentaenoic acid of the increases in nasal mucosal blood flow and eosinophilia of ryegrass-allergic reactions.

Nasal mucosal blood flow, assessed by a laser Doppler probe technique, and the concentration of eosinophils in nasal secretions were quantified during challenge of one nostril with ryegrass-pollen antigen and the other nostril with diluent alone in seven patients with ryegrass-allergic rhinitis. The identical studies were repeated after an 8-week course of 3.5 gm/day of eicosapentaenoic acid (EPA). Ryegrass antigen evoked mean rises in nasal blood flow of 30% to 100% after 10 and 30 minutes that were significant, relative to prechallenge levels and to levels after diluent challenge, both before and after EPA. Antigen-induced increases in nasal blood flow were significantly less after than before EPA at 10 minutes, and at 180 minutes increases were significant only before EPA. In ryegrass-allergic patients with rhinitis who did not take EPA between the two studies, the increases in blood flow after antigen challenge were the same on both occasions. Similarly, the nasal eosinophilia elicited by antigen was significant at 180 minutes only before EPA. Both a composite index of signs and symptoms and the constituent variables, reflecting the clinical response to antigen challenge, were unaffected by EPA. The suppression by EPA of responses of nasal blood flow and nasal eosinophils to antigen challenge supports a role for fatty acid and phospholipid mediators in allergic rhinitis, but the clinical assessment did not provide evidence for any symptomatic benefit from EPA.

Effect of eicosapentaenoic acid in asthma.

The role of arachidonic acid metabolites in the pathogenesis of airway inflammation and clinical asthma is currently unknown. The addition of eicosapentaenoic acid (EPA) to the diet of humans has been shown to generate metabolites that are less potent than their arachidonic acid counterparts. The substitution of EPA for arachidonic acid metabolites in patients might cause a decrease in airway inflammation and an improvement in clinical asthma. We studied the effect of addition of EPA to the diet of twelve asthmatic patients. Standard clinical evaluations and pulmonary function tests were done on weeks 0, 3, 6, 10, 12 and 14. Patients ingested either low-dose EPA (0.1 g/day) or high-dose EPA (4.0 g/day) from weeks 6-14 (total of 8 weeks). There was no difference in clinical status or pulmonary function between groups at the start of the study. There was no change in clinical status or pulmonary function between or within groups at the end of 8 weeks of EPA ingestion.

Alterations in human leukocyte function induced by ingestion of eicosapentaenoic acid.

Two groups of six adults with persistent asthma, who were identical clinically, received 0.1 or 4 g of purified eicosapentaenoic acid ethyl ester (EPA) daily for 8 weeks. Both doses increased significantly the generation of leukotriene B5 (LTB5) from EPA by polymorphonuclear (PMN) and mononuclear leukocytes, while only the high dose decreased leukocyte arachidonic acid (AA) and the generation of LTB4 and prostaglandin E2 from AA. Only the high dose led to inhibition of PMN leukocyte chemotaxis to multiple stimuli by a mean of 57-70% (P less than 0.01), without altering monocyte chemotaxis, the production of platelet-activating factor by mononuclear leukocytes, or the IgE-dependent release of histamine from basophils. Both doses of EPA increased the responses of T lymphocytes to phytohemagglutinin by a mean of 73% or more (P less than 0.01) without modifying the numbers of helper and suppressor T lymphocytes. EPA affects the functions of several types of leukocytes critical to inflammation and immunity.