Reply to Eisenhut

Abstract

injury. This study revealed that that eHSP72 was present in plasma and pulmonary edema fluid of acute lung injury patients and that eHSP72 was significantly higher in pulmonary edema fluid from patients with preserved alveolar epithelial fluid clearance. Furthermore, HSP activation in vivo in mice following heat stress or chemical HSP stimulation and in vitro in lung endothelial, epithelial, and macrophage cells caused intracellular expression and extracellular release of HSP72. Finally, HSP activation, but not eHSP72 itself, prevented the decrease in alveolar epithelial ion transport induced by exposure to IL-1. It is possible that the intracellular effect of HSP activation on inflammatory mediator expression and possibly regulation of NF-B activation may play a role in this positive effect on lung edema formation. It is likely that eHSP72 functions as a marker for enhanced intracellular HSP expression rather then as an active mediator of lung edema. Thus, although we agree pharmacological methods to control lung edema such as -agonists are clearly attractive areas of research, they only address one symptom of a global inflammatory lung injury process that will continue to injure the host. The potential for manipulation of HSP expression to appropriately regulate the immune response (perhaps via attenuated NF-B activation) and protect the organism’s cells from injury and death is clearly a more attractive option in attempting to improve clinical outcome from lung injury due to sepsis, trauma, and other inflammatory injuries.