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Open Access Research article

Demonstration of early functional compromise of bone marrow derived hematopoietic progenitor cells during bovine neonatal pancytopenia through in vitro culture of bone marrow biopsies

Eleanor Laming1, Eleonora Melzi1, Sandra FE Scholes2, Maira Connelly1, Charlotte R Bell3, Keith T Ballingall1, Mark P Dagleish1, Mara S Rocchi1 and Kim Willoughby1*

Author Affiliations

1 Moredun Research Institute, International Research Centre, Pentlands Science Park, Bush Loan, Midlothian, EH26 0PZ, UK

2 Animal Health and Veterinary Laboratories Agency Lasswade, Midlothian, UK

3 The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian, EH25 9RG, Scotland, UK

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BMC Research Notes 2012, 5:599  doi:10.1186/1756-0500-5-599

Published: 30 October 2012

Abstract

Background

Bovine neonatal pancytopenia (BNP) is a syndrome characterised by thrombocytopenia associated with marked bone marrow destruction in calves, widely reported since 2007 in several European countries and since 2011 in New Zealand. The disease is epidemiologically associated with the use of an inactivated bovine virus diarrhoea (BVD) vaccine and is currently considered to be caused by absorption of colostral antibody produced by some vaccinated cows (“BNP dams”). Alloantibodies capable of binding to the leukocyte surface have been detected in BNP dams and antibodies recognising bovine MHC class I and β-2-microglobulin have been detected in vaccinated cattle. In this study, calves were challenged with pooled colostrum collected from BNP dams or from non-BNP dams and their bone marrow hematopoietic progenitor cells (HPC) cultured in vitro from sternal biopsies taken at 24 hours and 6 days post-challenge.

Results

Clonogenic assay demonstrated that CFU-GEMM (colony forming unit-granulocyte/erythroid/macrophage/megakaryocyte; pluripotential progenitor cell) colony development was compromised from HPCs harvested as early as 24 hour post-challenge. By 6 days post challenge, HPCs harvested from challenged calves failed to develop CFU-E (erythroid) colonies and the development of both CFU-GEMM and CFU-GM (granulocyte/macrophage) was markedly reduced.

Conclusion

This study suggests that the bone marrow pathology and clinical signs associated with BNP are related to an insult which compromises the pluripotential progenitor cell within the first 24 hours of life but that this does not initially include all cell types.

Keywords:
Bovine neonatal pancytopaenia; BNP; Colostrum hematopoietic progenitor cells; BM-HPCs; Pluripotential