Bindu Nanduri, Ph.D.
Department of Basic Sciences
College of Veterinary Medicine
PO Box 6100
Mississippi State, MS 39762-6100
- M.S., Biosciences
University of Rookee, Roorkee, India.
- Ph.D., Biochemistry and Molecular Biology
University of Arkansas for Medical Sciences, Little Rock, Arkansas.
- Postdoctoral Research Associate
University of Arkansas for Medical Sciences, Little Rock, Arkansas
University of Medicine and Dentistry of New Jersey, Newark, NJ.
Mississippi State University, Mississippi State, MS.
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.
Another area of interest is to identify and characterize the role of iron responsive genes in pneumococcal virulence. Iron is a critical cofactor known to regulate gene expression in bacterial pathogens. Streptococcus pneumoniae colonizes the upper respiratory mucosa and has to adapt to lung and blood microenvironment during invasion. All these anatomic sites have varying concentrations of iron. A putative iron-dependent transcriptional regulator (IDTR) has been identified in S. pneumoniae TIGR4. A deletion mutant of idtr (Δidtr) is attenuated in mouse models of colonization, pneumonia and sepsis. We are currently exploring host innate immune mechanisms as well as pneumococcal gene expression in response to iron restriction.
My NSF EPSCoR research focuses on developing computational platforms to analyze dual-RNA-Seq expression data in co-infection models. We are also evaluating biological response to nano particles using proteomics in zebra fish models.