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2015 ; 9
(9
): e0004046
Nephropedia Template TP
PLoS Negl Trop Dis
2015[Sep]; 9
(9
): e0004046
PMID26393347
show ga
Buruli ulcer, an emerging tropical disease caused by Mycobacterium ulcerans (MU),
is characterized by disfiguring skin necrosis and high morbidity. Relatively
little is understood about the mode of transmission, pathogenesis, or host immune
responses to MU infection. Due to significant reduction in quality of life for
patients with extensive tissue scarring, and that a disproportionately high
percentage of those affected are disadvantaged children, a Buruli ulcer vaccine
would be greatly beneficial to the worldwide community. Previous studies have
shown that mice inoculated with either M. bovis bacille Calmette-Guérin (BCG) or
a DNA vaccine encoding the M. ulcerans mycolyl transferase, Ag85A (MU-Ag85A), are
transiently protected against pathology caused by intradermal challenge with MU.
Building upon this principle, we have generated quality-controlled,
live-recombinant strains of BCG and M. smegmatis which express the immunodominant
MU Ag85A. Priming with rBCG MU-Ag85A followed by an M. smegmatis MU-Ag85A boost
strongly induced murine antigen-specific CD4+ T cells and elicited functional
IFN?-producing splenocytes which recognized MU-Ag85A peptide and whole M.
ulcerans better than a BCG prime-boost vaccination. Strikingly, mice vaccinated
with a single subcutaneous dose of BCG MU-Ag85A or prime-boost displayed
significantly enhanced survival, reduced tissue pathology, and lower bacterial
load compared to mice vaccinated with BCG. Importantly, this level of superior
protection against experimental Buruli ulcer compared to BCG has not previously
been achieved. These results suggest that use of BCG as a recombinant vehicle
expressing MU antigens represents an effective Buruli ulcer vaccine strategy and
warrants further antigen discovery to improve vaccine efficacy.
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