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-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.
Garekar
Swati
S
Department of Pediatrics, Children's Hospital of Michigan, Wayne State University, Detroit, Michigan 48201, USA.
Heidemann
Sabrina M
SM
Glibetic
Maria
M
D000818:Animals; D002452:Cell Count; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D054426:Chemokine CXCL2; D018882:Heat Stress Disorders / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology / Q000633:toxicity*; D008264:Macrophages / Q000187:drug effects / Q000502:physiology; D051379:Mice; D015846:Monokines / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000302:isolation & purification; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D054426:Chemokine CXCL2; D008070:Lipopolysaccharides; D015846:Monokines; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha