Abstract
Vaccination with plasmid DNA encoding Ag85A from M. bovis BCG can partially protect C57BL/6 mice against a subsequent footpad challenge with M. ulcerans. Unfortunately, this cross-reactive protection is insufficient to completely control the infection. Although genes encoding Ag85A from M. bovis BCG (identical to genes from M. tuberculosis) and from M. ulcerans are highly conserved, minor sequence differences exist, and use of the specific gene of M. ulcerans could possibly result in a more potent vaccine. Here we report on a comparison of immunogenicity and protective efficacy in C57BL/6 mice of Ag85A from M. tuberculosis and M. ulcerans, administered as a plasmid DNA vaccine, as a recombinant protein vaccine in adjuvant or as a combined DNA prime-protein boost vaccine. All three vaccination formulations induced cross-reactive humoral and cell-mediated immune responses, although species-specific Th1 type T cell epitopes could be identified in both the NH2-terminal region and the COOH-terminal region of the antigens. This partial species-specificity was reflected in a higher—albeit not sustained—protective efficacy of the M. ulcerans than of the M. tuberculosis vaccine, particularly when administered using the DNA prime-protein boost protocol.
Highlights
Buruli ulcer (BU), known as Bairnsdale ulcer, is an infectious, necrotizing skin disease caused by Mycobacterium ulcerans (M. ulcerans) occurring mostly in tropical and subtropical areas
Buruli ulcer (BU) is an infectious disease characterized by deep, ulcerating skin lesions, on arms and legs, that are provoked by a toxin
Species-specific Th1 type cytokine production in spleen cell cultures from B6 mice vaccinated with Ag85ADNA, Ag85A protein or with a DNA prime-protein boost
Summary
Buruli ulcer (BU), known as Bairnsdale ulcer, is an infectious, necrotizing skin disease caused by Mycobacterium ulcerans (M. ulcerans) occurring mostly in tropical and subtropical areas. Cases have been reported in several countries in West and Central Africa, in Central and South America, in Southeast Asia and in Australia. BU is emerging as a serious health problem, especially in West Africa, where it is the third leading cause of mycobacterial disease in immunocompetent people, after tuberculosis and leprosy. In some countries in Africa, thousands of cases occur annually and in these areas BU has supplanted leprosy to become the second most important human mycobacterial disease. The natural history of M. ulcerans infection and subsequent development of BU is not completely elucidated. The infection causes initially a painless nodular swelling which can eventually develop into an extensive necrotizing lesion. ML suppresses the in vitro TNF-a production by murine macrophages infected with M. ulcerans (4)
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