Article Text

Recombinant Plasma Gelsolin Diminishes the Acute Inflammatory Response to Hyperoxia in Mice
  1. Melpo Christofidou-Solomidou,
  2. Arnaud Scherpereel,
  3. Charalambos C Solomides,
  4. Jason D Christie,
  5. Thomas P Stossel,
  6. Susan Goelz,
  7. Mark J DiNubile
  1. From the Divisions of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pennsylvania Medical School (M.C.-S., A.S., J.D.C.), Philadelphia
  2. Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School (T.P.S.), Boston, Mass
  3. Division of Infectious Diseases, Department of Medicine, Cooper Health System, UMDNJ/Robert Wood Johnson Medical School (M.J.D.), Camden, NJ
  4. Department of Pathology, Temple University School of Medicine (C.C.S.), Philadelphia, Pa
  5. Biogen, Inc (S.G.), Cambridge, Mass.
  1. Supported in part by American Heart Association grant no. 0030192N to M.C.-S.
  2. Address correspondence to: Mark DiNubile, MD, Associate Director of Clinical Research Publications (Infectious Diseases), Merck Research Laboratories, PO Box 4, BL3-4, West Point, PA 19486. E-mail mark_dinubile{at}


Background The acute respiratory distress syndrome remains a common and poorly understood complication of a variety of insults. Ventilation with high concentrations of inspired oxygen may further damage already compromised lungs. By scavenging extracellular actin and modulating the effects of lysophosphatidic acid, plasma gelsolin could serve a critical protective role against oxidant injury.

Methods Mice exposed to >95% O2 for a total of 72 hours were treated with gelsolin or albumin after 24 and 48 hours.

Results Neutrophil counts in bronchoalveolar fluid rose (P=0.0002) and gelsolin levels dropped (P<0.00001) in mice with acute hyperoxic lung injury. The acute inflammatory response to hyperoxia was significantly reduced in the gelsolin-compared with the bovine serum albumin-treated mice (P=0.03).

Conclusions These data imply that i) gelsolin depletion contributes to the pathogenesis of oxygen toxicity and ii) repletion of gelsolin can partially abrogate the resultant exudative response.

Key Words
  • gelsolin
  • hyperoxia
  • acute lung injury
  • inflammation
  • actin

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