Research article

Host immunity in the protective response to vaccination with heat-killed Burkholderia mallei

Gregory C Whitlock^1,2 , Roman A Lukaszewski⁶ , Barbara M Judy³ , Slobodan Paessler^4,5 , Alfredo G Torres^1,4,5 and D Mark Estes^1,3,5

¹  Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA

²  Department of Clinical Laboratory Sciences, University of Texas Medical Branch, Galveston, Texas, USA

³  Department of Pediatrics, University of Texas Medical Branch, Galveston, Texas, USA

⁴  Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA

⁵  Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas, USA

⁶  DSTL Biomedical Sciences, Porton Down, Salisbury, Wiltshire, SP4 0JQ, UK

author email corresponding author email

BMC Immunology 2008, 9:55doi:10.1186/1471-2172-9-55

Published:	29 September 2008

Abstract

Background

We performed initial cell, cytokine and complement depletion studies to investigate the possible role of these effectors in response to vaccination with heat-killed Burkholderia mallei in a susceptible BALB/c mouse model of infection.

Results

While protection with heat-killed bacilli did not result in sterilizing immunity, limited protection was afforded against an otherwise lethal infection and provided insight into potential host protective mechanisms. Our results demonstrated that mice depleted of either B cells, TNF-α or IFN-γ exhibited decreased survival rates, indicating a role for these effectors in obtaining partial protection from a lethal challenge by the intraperitoneal route. Additionally, complement depletion had no effect on immunoglobulin production when compared to non-complement depleted controls infected intranasally.

Conclusion

The data provide a basis for future studies of protection via vaccination using either subunit or whole-organism vaccine preparations from lethal infection in the experimental BALB/c mouse model. The results of this study demonstrate participation of B220⁺ cells and pro-inflammatory cytokines IFN-γ and TNF-α in protection following HK vaccination.