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

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Abstract
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-α) produced infiltration mainly of monocytes/macrophages in liver and heart; endothelial cell damage was absent in lung and heart and minimal in liver. Interleukin-1α (IL-1α) 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-α, and IL-1α, VLS was minimal and parenchymal and endothelial cell damage were less severe than after IL-2 alone or IL-2 plus IFN-α. Taken together, these observations show that IL-1α reduces ultrastructural changes produced by IL-2 and IFN-α. This reduction may be clinically useful in the treatment of neoplasms.

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