title: Ames hypopituitary dwarf mice demonstrate imbalanced myelopoiesis between bone marrow and spleen.
abstract: Ames hypopituitary dwarf mice are deficient in growth hormone, thyroid-stimulating hormone, and prolactin. The phenotype of these mice demonstrates irregularities in the immune system with skewing of the normal cytokine milieu towards a more anti-inflammatory environment. However, the hematopoietic stem and progenitor cell composition of the bone marrow (BM) and spleen in Ames dwarf mice has not been well characterized. We found that there was a significant decrease in overall cell count when comparing the BM and spleen of 4-5 month old dwarf mice to their littermate controls. Upon adjusting counts to differences in body weight between the dwarf and control mice, the number of granulocyte-macrophage progenitors, confirmed by immunophenotyping and colony-formation assay was increased in the BM. In contrast, the numbers of all myeloid progenitor populations in the spleen were greatly reduced, as confirmed by colony-formation assays. This suggests that there is a shift of myelopoiesis from the spleen to the BM of Ames dwarf mice; however, this shift does not appear to involve erythropoiesis. The reasons for this unusual shift in spleen to marrow hematopoiesis in Ames dwarf mice are yet to be determined but may relate to the decreased hormone levels in these mice.
authors.affiliation: Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
authors.forename: Maegan L
authors.initials: ML
authors.lastname: Capitano
authors.affiliation: Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
authors.forename: Brahmananda R
authors.initials: BR
authors.lastname: Chitteti
authors.affiliation: Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA.
authors.forename: Scott
authors.initials: S
authors.lastname: Cooper
authors.affiliation: Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.
authors.forename: Edward F
authors.initials: EF
authors.lastname: Srour
authors.affiliation: Department of Internal Medicine, Geriatrics Research, Southern Illinois University School of Medicine, Springfield, IL, USA.
authors.forename: Andrzej
authors.initials: A
authors.lastname: Bartke
authors.affiliation: Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA. Electronic address: hbroxmey@iupui.edu.
authors.forename: Hal E
authors.initials: HE
authors.lastname: Broxmeyer
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000276:immunology / Q000473:pathology*; D002452:Cell Count; D003433:Crosses, Genetic; D004392:Dwarfism / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D005260:Female; D005269:Femur / Q000276:immunology / Q000473:pathology; D015870:Gene Expression; D013006:Growth Hormone / Q000172:deficiency / Q000235:genetics / Q000276:immunology; D006412:Hematopoietic Stem Cells / Q000276:immunology / Q000473:pathology; D007018:Hypopituitarism / Q000235:genetics / Q000276:immunology / Q000473:pathology*; D016130:Immunophenotyping; D008297:Male; D051379:Mice; D016688:Mice, Inbred NOD; D016513:Mice, SCID; D008822:Mice, Transgenic; D022423:Myeloid Cells / Q000276:immunology / Q000473:pathology*; D038042:Myelopoiesis / Q000235:genetics / Q000276:immunology*; D011388:Prolactin / Q000172:deficiency / Q000235:genetics / Q000276:immunology; D013154:Spleen / Q000276:immunology / Q000473:pathology*; D013972:Thyrotropin / Q000172:deficiency / Q000235:genetics / Q000276:immunology
chemical_list: D011388:Prolactin; D013972:Thyrotropin; D013006:Growth Hormone
keywords: Ames dwarf mice; Growth hormone; Hematopoietic progenitor cell; Prolactin; Thyroid-stimulating hormone