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15 February 2007

Volume 195, Number 4
The Journal of Infectious Diseases 2007;195:581–584
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2007/19504-0016$15.00
DOI: 10.1086/510626
BRIEF REPORT

Hypersusceptibility to Invasive Pneumococcal Infection in Experimental Sickle Cell Disease Involves Platelet‐Activating Factor Receptor

Martha L. Miller,1

Geli Gao,1

Tamara Pestina,2

Derek Persons,2 and

Elaine Tuomanen1

1Department of Infectious Diseases and 2Division of Experimental Hematology, Comprehensive Sickle Cell Center, St. Jude Children’s Research Hospital, Memphis Tennessee

Children with sickle cell disease have a 600‐fold increased incidence of invasive pneumococcal disease. Platelet‐activating factor receptor (PAFr) mediates pneumococcal invasion, and up‐regulation of PAFr on chronically activated endothelia could contribute to increased bacterial invasion. Mice transplanted with sickle cell bone marrow developed more extensive infection, and 57% died, compared with 16% of wild‐type mice. Histopathological analysis revealed that sickle cell mice expressed significantly more PAFr on endothelia and epithelia. Pharmacological blockade or genetic deletion of PAFr protected sickle cell mice from mortality. We conclude that PAFr plays an important role in hypersusceptibility to pneumococcal infection in sickle cell disease.

Received 5 July 2006; accepted 20 September 2006; electronically published 8 January 2007.

Reprints or correspondence: Elaine I. Tuomanen, Dept. of Infectious Diseases, St. Jude Children’s Research Hospital, 332 N. Lauderdale St., Memphis, TN 38105 ().

Cited by

Ernesto Hinojosa, Angela R. Boyd, and Carlos J. Orihuela. Age‐Associated Inflammation and Toll‐Like Receptor Dysfunction Prime the Lungs for Pneumococcal Pneumonia. The Journal of Infectious Diseases 0:0, 000-000
Abstract-Full Text-PDF Version (460 kB)

  • Potential conflicts of interest: none reported.

    Financial support: National Institutes of Health (grants AI 27913 and AI 39482); National Heart, Lung, and Blood Institute (grant U54HL070590); American Lebanese Syrian Associated Charities.

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