My primary area of interest is to study host-pathogen interactions that underscore infectious diseases. We use functional genomics tools such as proteomics and RNA-Seq to study genome response to perturbation, both biotic and abiotic. My ongoing NIH COBRE funded research project focuses on studying the role of polyamines in pneumococcal pathogenesis using RNA-Seq and modeling the genome response in a systems biology framework. Streptococcus pneumoniae is the most common cause of community acquired pneumonia and the leading cause of meningitis, sinusitis, chronic bronchitis, and otitis media. Serotype variability, genomic plasticity and increasing antibiotic resistance of S. pneumoniae, pose considerable challenges for designing intervention strategies for this global public health concern. There is a need to identify and characterize novel vaccine candidates for effective immunization against pneumococcus, as the available vaccines are not effective against all serotypes. Polyamines are ubiquitous small cationic molecules necessary for pneumococcal growth and virulence. Intracellular polyamine levels are tightly regulated, thus making polyamine transport mechanisms highly attractive to investigate the pathogenesis and immune responses. Polyamine transport genes are conserved within the species and provide a potential new class of broad-based vaccine candidates or therapeutic targets. We showed that impaired polyamine transport causes attenuation of pneumonia in mouse models. Our long term goal is to characterize the pathogen specific pathways and the host immune responses responsible for this attenuation.
