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, Helene F. Rosenberg

Research output: Contribution to journalArticlepeer-review

138 Scopus citations


We explore the controversial issue of the role of eosinophils in host defense against helminthic parasites using the established Schistosoma mansoni infection model in 2 novel mouse models of eosinophil lineage ablation (ΔdblGATA and TgPHIL). No eosinophils were detected in bone marrow of infected ΔdblGATA or TgPHIL mice, despite the fact that serum IL-5 levels in these infected mice exceeded those in infected wild type by approximately 4-fold. Liver granulomata from infected ΔdblGATA and TgPHIL mice were likewise depleted of eosinophils compared with 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 ΔdblGATA 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 eosinophil ablation has 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.

Original languageEnglish (US)
Pages (from-to)2420-2427
Number of pages8
Issue number7
StatePublished - Oct 1 2006

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology


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