Role for interleukin‐1 in the pathogenesis of hypersensitivity diseases

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Abstract
Interleukin‐1 (IL‐1), a polypeptide product of various cells, is one of the key mediators of the body's response to microbial invasion, inflammation, immunological reactions, and tissue injury. IL‐1 is a prominent member of a group of polypeptide mediators now called “cytokines.” Current evidence suggests that IL‐1 is not produced in health but that any perturbation such as inflammation or even slight injury triggers the expression of IL‐1 genes. The biological effects of IL‐1 are manifested in nearly every tissue and organ. These include various proinflammatory effects such as increased production of arachidonate metabolites, synovial cell proteases, activation of basophils, eosinophils and neutrophils, endothelial cell adhesiveness, and stimulation of lymphocyte responses. Control of IL‐1 synthesis in certain diseases is often appropriate. Although corticosteroids reduce both the transcription and translation of IL‐1, we have recently investigated the effect of dietary supplementation with N‐3 (omega‐3) fatty acids in human volunteers. The results indicate that increasing the amount of N‐fatty acids in the diet decreases the ability of blood mononuclear cells to synthesize IL‐1 in vitro. It is suggested that the ameliorative effects of N‐3 fatty acid dietary supplements in patients with hypersensitive diseases may be, in part, the result of decreased IL‐1 production.