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Interleukin-1-Mediated Acute Lung Injury

  • B. M. Hybertson
  • J. E. Repine
Conference paper
  • 91 Downloads
Part of the Yearbook of Intensive Care and Emergency Medicine book series (YEARBOOK, volume 1997)

Abstract

The acute respiratory distress syndrome (ARDS) is a highly fatal form of acute lung injury (ALI) for which no effective therapy is currently available. Despite the fact that ARDS was first described more than 25 years ago, its etiology remains essentially unknown. Furthermore, because of the diverse variety of predisposing insults for the development of ARDS, the existence of complex pathogenetic pathways appears likely. A unifying, and perhaps a common hypothesized mechanism is that pro-inflammatory mediators, neutrophils, and reactive oxygen species contribute to the development of ARDS. Some of the evidence for this premise can be summarized as follows:
  • ARDS patients have increased numbers of neutrophils in their lungs, and these neutrophils are potent sources of oxygen radicals [1, 2];

  • ARDS patients have elevated levels of the pro-inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor-α (TNF) in their bronchoalveolar lavage (BAL) fluid and have alveolar macrophages that release increased amounts of IL-1 [3–5];

  • ARDS patients have increased lung lavage levels of factors such as IL-8 that can attract and stimulate neutrophils [4–10];

  • Neutrophils recovered from the blood or lungs of ARDS patients have altered functional activity, suggesting that they have been exposed to neutrophil activating factors [11, 12];

  • Stimulated neutrophils damage isolated perfused lung and lung endothelial cell monolayers [13, 14];

  • ARDS patients have increased plasma levels of xanthine oxidase, which can generate oxygen radicals [15];

  • ARDS patients have an increased burden of endogenous oxidants as evidenced by increased concentrations of hydrogen peroxide in their exhaled breaths [16, 17], increased levels of lipid peroxidation products in their blood [18], and increased levels of oxidized antiproteases in their lung lavage fluid [19]; and

  • ARDS patients have decreased levels of the antioxidants glutathione and vitamin E in their lung lavage fluid and plasma [18, 20].

Keywords

Lung Injury Acute Lung Injury Acute Respiratory Distress Syndrome Adult Respiratory Distress Syndrome Acute Respiratory Distress Syndrome Patient 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • B. M. Hybertson
  • J. E. Repine

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