In VivoHyperthermia Enhances Plasma Antiviral Activity and Stimulates Peripheral Lymphocytes for Increased Synthesis of Interferon-γ

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Abstract
The effect of in vivo hyperthermia on plasma interferon (IFN) activity and on the induction of IFN-γ by phytohemagglutinin (PHA) or staphylococcal enterotoxin B (SEB) in isolated leukocyte cultures was investigated. Adult rhesus monkeys (Macaca mulatta) were placed in a climatic chamber maintained at 45°C until their core body temperatures increased 2°C above control levels. Peripheral blood samples were withdrawn both prior to core temperature elevation and at the time of peak body temperature. Plasma IFN-α increased slightly from a control value of 12 U/ml to 16 U/ml at the elevated core temperature. However, this alteration of plasma IFN levels appears to be a complex process that includes the loss of certain circulating IFN-α subtypes and the influx of acid-labile (Type II) IFN-α. Additionally, a non-IFN antiviral factor present in the plasma was elevated 10-fold at the higher body temperature. When mononuclear cells were isolated and cultured at 37°C in the presence of PHA or SEB, those cells isolated from animals at the peak of body temperature showed a 4- to 16-fold increase in IFN-γ activity relative to cells isolated from the same animal before the temperature increase. Similar results were obtained with cells isolated when fever was induced by the systemic injection of nonviable Escherichia coli. These results demonstrate that increased body temperature results in a circulating lymphocyte pool which is "primed" for the production of elevated levels of IFN-γ activity. We suggest that the physiologically complex response of fever involves a fundamental alteration in circulating lymphocytes in a manner that can potentially augment the synthesis of IFN-γ.