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Hypersusceptibility to invasive pneumococcal infection in experimental sickle cell disease involves

Martha L Miller1, Geli Gao, Tamara Pestina

  • 1Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.

The Journal of Infectious Diseases
|January 19, 2007
PubMed

Insights

Sickle cell disease patients face higher risks of pneumococcal infections. Blocking the platelet-activating factor receptor (PAFr) significantly protected sickle cell model mice from severe disease and death.

Area of Science:

  • Infectious diseases
  • Hematology
  • Immunology

Background:

  • Children with sickle cell disease exhibit a 600-fold higher risk of invasive pneumococcal disease.
  • Platelet-activating factor receptor (PAFr) is implicated in pneumococcal invasion pathways.
  • Upregulation of PAFr on activated endothelial cells may enhance bacterial entry.

Purpose of the Study:

  • To investigate the role of PAFr in the increased susceptibility to pneumococcal infections in sickle cell disease.

Main Methods:

  • Mice with sickle cell bone marrow were compared to wild-type mice for infection severity and mortality.
  • Histopathological analysis assessed PAFr expression on endothelial and epithelial cells.
  • Pharmacological blockade and genetic deletion of PAFr were employed.

Main Results:

  • Sickle cell mice showed more extensive infections and a higher mortality rate (57%) compared to wild-type mice (16%).
  • Significantly increased PAFr expression was observed on endothelia and epithelia in sickle cell mice.
  • PAFr blockade or deletion conferred protection against mortality in sickle cell mice.

Conclusions:

  • PAFr plays a critical role in the heightened susceptibility to pneumococcal infections observed in sickle cell disease.
  • Targeting PAFr may offer a therapeutic strategy to mitigate pneumococcal disease severity in affected individuals.

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