Submitted December 1, 2005
Accepted May 29, 2006
Schistosoma mansoni infection in eosinophil
lineage-ablated mice
Jonathan M Swartz, Kimberly D Dyer, Allen W Cheever, Thirumalai Ramalingam, Lesley Pesnicak, Joseph B Domachowske, James J Lee, Nancy A Lee, Paul S Foster, Thomas A Wynn, and Helene F Rosenberg*
National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, USA
SUNY Upstate Medical University, Syracuse, NY, USA
Mayo Clinic Arizona, Scottsdale, Arizona, USA
Hunter Medical Research Institute, University of Newcastle, NSW, Australia
* Corresponding author; email: hrosenberg{at}niaid.nih.gov.
We explore the controversial issue of the role of eosinophils in host defense against helminthic parasites using the established Schistosoma mansoni infection model in two novel mouse models of eosinophil lineage ablation (
dblGATA and TgPHIL). No eosinophils were detected in bone marrow of infected dblGATA or TgPHIL mice, despite the fact that serum IL-5 levels in these infected mice exceeded those in infected wild type by ~ 4-fold. Liver granulomata from infected dblGATA and TgPHIL mice were likewise depleted of eosinophils compared to those from their respective wild types. No eosinophil-dependent differences in granuloma number, size, or fibrosis were detected at weeks 8 or 12 of infection, and differential accumulation of mast cells was observed among the dblGATA mice only at week 12. Likewise, serum levels of liver transaminases, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) increased in all mice in response to S. mansoni infection, with no eosinophil-dependent differences in hepatocellular damage observed. Finally, eosinophil ablation had no effect on worm burden or on egg deposition. Overall, our data indicate that eosinophils have no impact on traditional measures of disease in the S. mansoni infection model in mice. However, eosinophils may have unexplored immunomodulatory contributions to this disease process.
