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J Appl Physiol 97: 2005, 2004; doi:10.1152/japplphysiol.00920.2004
8750-7587/04 $5.00
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COMMENTARY

HIGHLIGHTED TOPICS
Lung Growth and Repair

Commentary

In the first featured article, entitled "Redistribution of pulmonary EC-SOD after exposure to asbestos," Drs. R. Tan and C. Fattman and colleagues (1) examine the role of extracellular superoxide dismutase (EC-SOD) in asbestos-mediated lung injury. EC-SOD is the predominant antioxidant enzyme in the extracellular matrix of the lung. These investigators found that exposure to asbestos causes EC-SOD to be redistributed in the mouse lung, leading to depleted supplies in the lung parenchyma and accumulation in the bronchoalveolar lavage fluid. The mechanism for redistribution appears to be proteolytic cleavage of the heparin-binding domain of EC-SOD, as most of the EC-SOD found in the bronchoalveolar lavage fluid is the proteolyzed form lacking this domain. This redistribution of EC-SOD from the lung parenchyma to the bronchoalveolar lavage fluid was associated with development of pulmonary fibrosis (asbestosis) 14 days after exposure to asbestos. Such redistribution of EC-SOD after asbestos-induced lung injury may contribute to the development of pulmonary fibrosis by intensifying the oxidant/antioxidant imbalance in the extracellular matrix of the lung, resulting in greater injury and impaired repair.

In the second featured article, entitled "Pentoxifylline reduces fibrin deposition and prolongs survival in neonatal hyperoxic lung injury," Dr. S. ter Horst and colleagues (2) explore the efficacy of pentoxifylline, a xanthine derivative and phosphodiesterase inhibitor, to suppress production of early mediators of inflammation and stimulate fibrinolysis in the lung. Ventilated preterm infants frequently develop bronchopulmonary dysplasia, a multifactorial, chronic lung disease characterized by arrested alveolarization and vascularization. Treating hyperoxia-exposed preterm rat pups with pentoxifylline diminished the severity of tissue damage by reducing capillary leakage of proteins, deposition of fibrin in the lung alveoli, expression of monocyte chemoattractant protein-1 in the lungs, and white blood cell counts in the bronchoalveolar lavage fluid. Most importantly, treatment with pentoxifylline prolonged survival. Pentoxifylline did not affect expression of tumor necrosis factor-{alpha} (TNF-{alpha}) or interleukin-6, its key proinflammatory targets in endotoxemia, suggesting that TNF-{alpha} does not play the same pivotal role in the inflammatory response in neonatal hyperoxia-induced lung injury as it does in endotoxemia. These observations are exciting because inflammation and coagulation are pivotal events not only in the lungs of ventilated preterm infants but also in the lungs of children and adults with acute respiratory distress syndrome.

Gary C. Sieck

Journal of Applied Physiology November 2004, Volume 97

REFERENCES

  1. Tan RJ, Fattman CL, Watkins SC, and Oury TD. Redistribution of pulmonary EC-SOD after exposure to asbestos. J Appl Physiol 97: 2006–2013, 2004.[Abstract/Free Full Text]
  2. Ter Horst SAJ, Wagenaar GTM, deBoer E, van Gastelen MA, Meijers JCM, Poorthuis BJHM, and Walther FJ. Pentoxifylline reduces fibrin deposition and prolongs survival in neonatal hyperoxic lung injury. J Appl Physiol 97: 2014–2019, 2004.[Abstract/Free Full Text]




This Article
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