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Infection and Immunity, October 2003, p. 5970-5978, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5970-5978.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Pneumocystis Pneumonia Increases the Susceptibility of Mice to Sublethal Hyperoxia

James M. Beck,1,2* Angela M. Preston,1 Steven E. Wilcoxen,1 Susan B. Morris,1 Eric S. White,1 and Robert Paine III1,2

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School ,1 Medical Service, Department of Veterans Affairs Medical Center, Ann Arbor, Michigan 481052

Received 9 May 2003/ Returned for modification 17 June 2003/ Accepted 8 July 2003

Patients with Pneumocystis pneumonia often develop respiratory failure after entry into medical care, and one mechanism for this deterioration may be increased alveolar epithelial cell injury. In vitro, we previously demonstrated that Pneumocystis is not cytotoxic for alveolar epithelial cells. In vivo, however, infection with Pneumocystis could increase susceptibility to injury by stressors that, alone, would be sublethal. We examined transient exposure to hyperoxia as a prototypical stress that does cause mortality in normal mice. Mice were depleted of CD4+ T cells and inoculated intratracheally with Pneumocystis. Control mice were depleted of CD4+ T cells but did not receive Pneumocystis. After 4 weeks, mice were maintained in normoxia, were exposed to hyperoxia for 4 days, or were exposed to hyperoxia for 4 days followed by return to normoxia. CD4-depleted mice with Pneumocystis pneumonia demonstrated significant mortality after transient exposure to hyperoxia, while all uninfected control mice survived this stress. We determined that organism burdens were not different. However, infected mice exposed to hyperoxia and then returned to normoxia demonstrated significant increases in inflammatory cell accumulation and lung cell apoptosis. We conclude that Pneumocystis pneumonia leads to increased mortality following a normally sublethal hyperoxic insult, accompanied by alveolar epithelial cell injury and increased pulmonary inflammation.

* Corresponding author. Mailing address: Pulmonary and Critical Care Medicine (111G), VA Medical Center, 2215 Fuller Rd., Ann Arbor, MI 48105. Phone: (734) 761-7980. Fax: (734) 761-5385. Email: jamebeck{at}umich.edu.

Editor: T. R. Kozel

Infection and Immunity, October 2003, p. 5970-5978, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5970-5978.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Beck, J. M., Preston, A. M., Wilcoxen, S. E., Morris, S. B., Sturrock, A., Paine, R. III (2009). Critical Roles of Inflammation and Apoptosis in Improved Survival in a Model of Hyperoxia-Induced Acute Lung Injury in Pneumocystis murina-Infected Mice. Infect. Immun. 77: 1053-1060 [Abstract] [Full Text]  
  • Christensen, P. J., Preston, A. M., Ling, T., Du, M., Fields, W. B., Curtis, J. L., Beck, J. M. (2008). Pneumocystis murina Infection and Cigarette Smoke Exposure Interact To Cause Increased Organism Burden, Development of Airspace Enlargement, and Pulmonary Inflammation in Mice. Infect. Immun. 76: 3481-3490 [Abstract] [Full Text]  
  • Baleeiro, C. E. O., Christensen, P. J., Morris, S. B., Mendez, M. P., Wilcoxen, S. E., Paine, R. III (2006). GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Am. J. Physiol. Lung Cell. Mol. Physiol. 291: L1246-L1255 [Abstract] [Full Text]  
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