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

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
The Journal of Infectious Diseases (Impact Factor: 6). 03/2007; 195(4):581-4. DOI: 10.1086/510626
Source: PubMed


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.

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