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Interleukin-la Reduces the Severity of the Vascular Leak Syndrome Produced by Interleukin-2 and Interleukin-2 Plus Interferon-a

Pathology Branch, National Heart Lung and Blood Institute, National Institutes of Health

Raj Puri

Division of Cytokine Biology, Center for Biologics Evaluation and Research, Food and Drug Administration

Zu-Xi Yu

Pathology Branch, National Heart Lung and Blood Institute, National Institutes of Health

William Travis

Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland 20892

Maria Yamaguchi

Pathology Branch, National Heart Lung and Blood Institute, National Institutes of Health

Victor J. Ferrans

Pathology Branch, National Heart Lung and Blood Institute, National Institutes of Health

Histological and ultrastructural changes were investigated in lung, liver, and heart of mice given interleukin-2 (IL-2), either alone or in combination with other cytokines. IL-2 induced a vascular leak syndrome (VLS) of a moderate degree with infiltration of lymphoid cells, moderate endothelial damage. mild hepatic parenchymal damage, and minimal myocardial alterations. Interferon-a (IFN-) produced infiltration mainly of monocytes/macrophages in liver and heart; endothelial cell damage was absent in lung and heart and minimal in liver. Interleukin-1 (IL-1) caused an increased number of neutrophils in liver and lung; VLS and parenchymal cell and endothelial damage were not found. The VLS and the cellular damage caused by the combination of IL-2 and IFN were much more severe than those produced by IL-2 alone. In animals treated with IL-2, IFN-, and IL-1, VLS was minimal and parenchymal and endothelial cell damage were less severe than after IL-2 alone or IL-2 plus IFN-. Taken together, these observations show that IL-1 reduces ultrastructural changes produced by IL-2 and IFN-. This reduction may be clinically useful in the treatment of neoplasms.

Key Words: Myocardium • liver • lung • endothelium • toxicity • ultrastructure • lymphocyte • macrophage

Toxicologic Pathology, Vol. 22, No. 4, 381-397 (1994)
DOI: 10.1177/019262339402200404


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