Abstract

Reye's syndrome is a serious childhood disease usually associated with an antecedent viral illness such as influenza or chicken pox. Recent reports indicate a relationship between moderate aspirin use during the viral infection and the development of Reye's disease. The blastogenic response of cultured lymphocytes to lectins mimics their in vivo response to viral antigens. We report here that physiological doses of the cyclooxygenase inhibitor aspirin, induce marked hyperactivity in this response. Mouse spleen lymphocyte cultures were treated with phytohemagglutinin (PHA) and mitogenesis was assayed after 72 hours by measuring incorporation of 3H thymidine. Addition of aspirin produced up to 3-fold increases in the PHA response. The effect was specific for T-lymphocytes and response to the B lymphocyte mitogen LPS was not significantly affected. The hyperproliferative effect was dose-dependent being maximum at aspirin levels of 300–400 μM and was reversed by addition of prostaglandin E 2 (10-9M). Maximum effects were observed when aspirin was added to cells within 8–10 hours of exposure to antigen. The observations suggest that Reye's syndrome may result from an aspirin-induced aberration in the immune response to a viral infection.

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