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Infection and Immunity, October 2008, p. 4414-4421, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00012-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Pseudomonas aeruginosa Induces Localized Immunosuppression during Pneumonia{triangledown} ,{dagger}

Maureen H. Diaz,1,{ddagger} Ciara M. Shaver,1,{ddagger},§ John D. King,1,¶ Srinidhi Musunuri,2,|| Jeffrey A. Kazzaz,3 and Alan R. Hauser1,4*

Department of Microbiology/Immunology, Northwestern University, Chicago, Illinois,1 Department of Pathology, Northwestern University, Chicago, Illinois,2 CardioPulmonary Research Institute and Division of Pulmonary and Critical Care Medicine, Winthrop Hospital University and State University of New York at Stony Brook, Mineola, New York,3 Department of Medicine, Northwestern University, Chicago, Illinois4

Received 4 January 2008/ Returned for modification 4 March 2008/ Accepted 18 July 2008

Hospital-acquired bacterial pneumonia is a common and serious complication of modern medical care. Many aspects of such infections remain unclear, including the mechanisms by which invading pathogens resist clearance by the innate immune response and the tendency of the infections to be polymicrobial. Here, we used a mouse model of infection to show that Pseudomonas aeruginosa, a leading cause of hospital-acquired pneumonia, interferes with the ability of recruited phagocytic cells to eradicate bacteria from the lung. Early in infection, phagocytic cells, predominantly neutrophils, are recruited to the lungs but are incapacitated when they enter the airways by the P. aeruginosa toxin ExoU. The resulting paucity of functioning phagocytes allows P. aeruginosa to persist within the lungs and results in local immunosuppression that facilitates superinfection with less-pathogenic bacteria. Together, our results provide explanations for previous reports linking ExoU-secreting P. aeruginosa with more severe pulmonary infections and for the tendency of hospital-acquired pneumonia to be polymicrobial.

* Corresponding author. Mailing address: 303 E. Chicago Ave., Searle 6-495, Chicago, IL 60611. Phone: (312) 503-1044. Fax: (312) 503-1339. E-mail: ahauser{at}northwestern.edu

{triangledown} Published ahead of print on 28 July 2008.

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Editor: B. A. McCormick

{ddagger} M.H.D. and C.M.S. contributed equally to this study.

§ Present address: Vanderbilt University Medical Center, Department of Internal Medicine, D-3100, Nashville, TN.

Present address: Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5307.

|| Present address: Condell Pathology Group, Libertyville, IL.

Infection and Immunity, October 2008, p. 4414-4421, Vol. 76, No. 10
0019-9567/08/$08.00+0     doi:10.1128/IAI.00012-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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