Heat shock response, heat shock proteins, and acute lung injury

Hyon Lee, Micaela Godzich, Jean François Pittet

Research output: Chapter in Book/Report/Conference proceedingChapter

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, H2 O2, 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.

Original languageEnglish (US)
Title of host publicationAcute Respiratory Distress Syndrome
PublisherCRC Press
Pages254-274
Number of pages21
ISBN (Electronic)9780203912034
ISBN (Print)9780824740764
StatePublished - Jan 1 2003
Externally publishedYes

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ASJC Scopus subject areas

  • Medicine(all)

Cite this

Lee, H., Godzich, M., & Pittet, J. F. (2003). Heat shock response, heat shock proteins, and acute lung injury. In Acute Respiratory Distress Syndrome (pp. 254-274). CRC Press.