Heat stress response results in increased macrophage inflammatory protein-2 concentration in a lipopolysaccharide-exposed macrophage cell line

Pretreatment with heat confers cardiopulmonary protection in endotoxemic animals. This mechanism may be through suppression of pro-inflammatory mediator production. The objectives of this study were to determine the effect of heat stress on tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein-2 (MIP-2) in a lipopolysaccharide-exposed macrophage cell line and to study the relationship between TNF-α and MIP-2 production. Heat pretreatment resulted in decreased TNF-α transcription and translation by lipopolysaccharide-exposed macrophages; and increased MIP-2 concentration without additional effect in transcription. Administration of TNF-α antibody prior to exposure to lipopolysaccharide resulted in increased MIP-2 concentration suggesting that TNF-α acts to down-regulate MIP-2 production. The mechanism by which heat stress causes an increase in MIP-2 concentration may be secondary to its suppressing effect on TNF-α production.