The primary research focus of my work is in the area of signaling and immunology in mouse model of tuberculosis that involves investigating the role of antimicrobial peptides in tuberculosis infection and control. I am also working to dissect the role of cyclic AMP signaling pathway which intoxicates and alters the cellular response to Mycobacterium tuberculosis infection by modulating host cell signaling events to promote an environment favorable for mycobacterial growth and survival. My studies with Mycobacterium tuberculosis will help understand the underlying mechanisms of host-pathogen interaction and other pathways involved during tuberculosis with special focus on mycobacterial pathogenesis.
Another interesting aspect that I am working on is the role of efflux during tuberculosis treatment. My recent studies have shown that verapamil, which is an efflux inhibitor, can be used to accelerate both the bactericidal and the sterilizing activity of standard tuberculosis treatment. Using pharmacokinetic parameters for verapamil, we have also determined that a dose adjustment of verapamil is required to compensate for concurrent use of rifampin during tuberculosis treatment. We have also shown that concurrent use of verapamil with latest FDA approved drug bedaquiline (TMC207) can potentiate latter’s activity. The goal of the study is to employ this understanding towards improved drug regimens for tuberculosis control.