Heat stress decreases pulmonary MCP-1 production in endotoxemia.

An exaggerated pro-inflammatory response in endotoxemia may lead to multiple organ damage including acute lung injury. Heat stress prior to endotoxemia results in attenuation of inflammation possibly by decreasing cytokine production. Monocyte chemoattractant protein (MCP)-1, a pro-inflammatory cytokine, is responsible for monocyte recruitment into the lung in acute lung injury. The objective of this study is to determine if pretreatment with heat results in decreased MCP-1 production in the lungs of endotoxemic rats at a transcriptional or post-transcriptional level. Rats were assigned to one of four groups: control, heat alone, heat with or without endotoxin. Rats were made endotoxemic by injection of Escherichia coli lipopolysaccharide. MCP-1 was measured in lavage fluid and MCP-1 mRNA in the lung tissue. Endotoxemia resulted in production of MCP-1. Control and heat alone rats had 21+/-4 vs. 20+/-3 pg/ml, p=0.75. MCP-1 concentration was decreased in the lavage fluid of pre-heated when compared to non-heated endotoxemic rats (37+/-28 vs. 70+/-35 pg/ml, p <0.02 ). However, the MCP-1 mRNA was higher in the heated compared to non-heated endotoxemic rats (1.59+/-0.35 vs. 0.74+/-0.51, MCP-1/beta-actin mRNA, p <0.01). Control and heat alone rats had undetectable mRNA MCP-1 in the lungs. Heat stress prior to endotoxemia results in decreased production of MCP-1 by a post-transcriptional mechanism.