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

Swati Garekar

Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, Michigan, USA

Sabrina M. Heidemann

Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, Michigan, USA, sheidema{at}med.wayne.edu

Maria Glibetic

Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, Michigan, USA

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-{alpha} (TNF-{alpha}) and macrophage inflammatory protein-2 (MIP-2) in a lipopolysaccharide-exposed macrophage cell line and to study the relationship between TNF-{alpha} and MIP-2 production. Heat pretreatment resulted in decreased TNF-{alpha} transcription and translation by lipopolysaccharide-exposed macrophages; and increased MIP-2 concentration without additional effect in transcription. Administration of TNF-{alpha} antibody prior to exposure to lipopolysaccharide resulted in increased MIP-2 concentration suggesting that TNF-{alpha} 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-{alpha} production.

Key Words: Endotoxin • heat stress • macrophage • macrophage inflammatory protein-2 • tumor necrosis factor-{alpha}

Journal of Endotoxin Research, Vol. 12, No. 2, 87-92 (2006)
DOI: 10.1177/09680519060120020401
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