Increased protection and decreased lung immunopathology induced by the ID93/GLA-SE vaccine candidate following infection with Mycobacterium tuberculosis HN878.

Abstract Mycobacterium tuberculosis (M. tuberculosis) HN878 causes death and extensive lung pathology in infected C57BL/6 mice. A clinically relevant isolate of M. tuberculosis increases the possibilities of assessing the efficacy of experimental TB vaccines against human TB strains in a relatively inexpensive and immunologically intact small animal model. This model will also allow for the measurement of survival in mice and hence the determination of long-lived effects of M. tuberculosis vaccines. In this study, we show that the ID93/GLA-SE tuberculosis vaccine candidate elicits protection against M. tuberculosis HN878 by reducing the bacterial burden in the lung and spleen, and prevents the extensive lung pathology that is induced by M. tuberculosis HN878 in C57BL/6 mice. Future studies utilizing this model will allow the use of specific knock-out mice on the C57BL/6 mouse background to critically examine key immunological factors that are responsible for long-lived, vaccine-induced immunity and prevention of pulmonary immunopathology induced by a virulent clinical isolate of M. tuberculosis.