ABSTRACT
The heat shock response was discovered in 1962 by Ritossa (1), who reported that Drosophila salivary gland chromosome puffs were induced in response to transient hyperthermia. Since this first observation, a large number of investigators have reported that this pattern was linked to the expression of a specific group of proteins called heat shock proteins. The expression of these proteins in response to hyperthermia was called the “stress response” or “heat shock response,” a ubiquitous and highly conserved defense mechanism in all organisms, from bacteria to animals and humans. The acute respiratory distress syndrome (ARDS) is a devastating syndrome of acute inflammation of the lung that affects both barriers of the lung-the lung endothelium and the alveolar epithelium (2). The early phase of acute lung injury is characterized by the accumulation of inflammatory cells (neutrophils, macrophages) within the alveolar structures that release high levels of oxidant species such as superoxide, H2O2, or reactive nitrogen species (2). One of the most important consequences associated with the induction of the heat shock response is to confer cytoprotection against a variety of stressors, such as oxidant-mediated injury, one of the most important molecular mechanisms of acute lung injury.
