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Original Research: Critical Care |

Tripeptide feG Prevents and Ameliorates Acute Pancreatitis-Associated Acute Lung Injury in a Rodent ModelfeG Prevents and Ameliorates Rodent Lung Injury

Alison S. F. Elder, PhD; Andrew D. Bersten, MD; Gino T. P. Saccone, PhD; Dani-Louise Dixon, PhD
Author and Funding Information

From the Departments of Critical Care Medicine (Drs Elder, Bersten, and Dixon), and Surgery (Dr Saccone), Flinders University, Adelaide, SA, Australia.

Correspondence to: Alison Elder, PhD, Department of Critical Care Medicine, Flinders University, GPO Box 2100, Adelaide, SA, Australia 5001; e-mail: a.elder@flinders.edu.au


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(2):371-378. doi:10.1378/chest.11-2868
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Background:  The synthetic tripeptide feG (D-Phe-D-Glu-Gly) is a novel pharmacologic agent that decreases neutrophil recruitment, infiltration, and activation in various animal models of inflammatory disease. We aimed to investigate the effect of feG as both a preventive treatment when administered before acute lung injury and as a therapeutic treatment administered following initiation of acute lung injury.

Methods:  Lung injury was assessed following prophylactic or therapeutic intratracheal feG administration in a “two-hit” rodent model of acute pancreatitis plus intratracheal lipopolysaccharide.

Results:  Following both prophylactic and therapeutic feG administration, there were significant improvements in arterial blood oxygenation and respiratory mechanics and decreased lung edema, BAL protein concentration, histologic tissue injury scores, BAL cell infiltration, and lung myeloperoxidase activity. Most indices of lung damage were reduced to baseline control values.

Conclusions:  feG reduced leukocyte infiltration, ameliorated the severity of inflammatory damage, and restored lung function when administered either prophylactically or therapeutically in a two-hit rat model of acute pancreatitis plus intratracheal lipopolysaccharide.

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