1. ¹Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA
2. ²Department of Pathology, Harvard Medical School, Boston, MA, USA
3. ³Department of Pediatrics and Child Health, Kurume University School of Medicine, Kurume City, Japan
4. ⁴Department of Anatomy, Chonbuk National University Medical School, Jeonju, Republic of Korea
5. ⁵Department of Biology, James Madison University, Harrisonburg, VA, USA
6. ⁶Department of Medicine, Dana-Farber Cancer Institute, Boston, MA, USA
7. ⁷Department of Medicine, Harvard Medical School, Boston, MA, USA
8. ⁸Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA

Correspondence: Dr SJ Galli, MD, Department of Pathology, Stanford University School of Medicine, L235, 300 Pasteur Drive, Stanford, CA 94305-5324, USA. E-mail: sgalli@stanford.edu

Received 17 May 2005; Revised 29 June 2006; Accepted 30 June 2006; Published online 7 August 2006.

Abstract

To evaluate the potential roles of Interleukin-3 (IL-3) and c-Kit, the tyrosine kinase receptor for stem cell factor (SCF), in eosinophil responses in vivo, we examined eosinophil numbers in uninfected or nematode-infected wild-type mice, IL-3-/- mice, and IL-3-/- mice that also have a marked reduction in SCF/c-Kit signaling (ie, Kit^W/Kit^W-v, IL-3-/- mice). We found no significant differences in the numbers of eosinophils in the blood, bone marrow or various tissues of IL-3-/- vs IL-3+/+ mice, either at baseline or after the induction of bone marrow, blood or tissue eosinophilia in response to infection with Strongyloides venezuelensis (S.v.) or Nippostrongylus brasiliensis (N.b.). However, in mice with markedly impaired SCF/c-Kit signaling, IL-3 contributed significantly to the increased numbers of eosinophils that were observed in multiple tissues during S.v. infection, but not during infection with N.b.