Chandra Shekhar Bakshi, D.V.M., Ph.D.
Chandra Shekhar Bakshi, D.V.M., Ph.D., leads a laboratory that is focused on understanding the immunopathogenesis of Francisella tularensis; the causative agent of tularemia. F. tularensis is classified as category A select agent by the CDC. One critical characteristic of F. tularensis is its ability to dampen or subvert the functions of cells involved in innate immune defenses. F. tularensis infection leads to rapid bacterial replication in the host. Despite an explosive increase in bacterial number, the activation of macrophages is markedly suppressed. In addition, F. tularensis exerts a profound suppressive effect on the induction of pro-inflammatory cytokines by restricting signal transduction pathways. By taking a comprehensive approach in the areas of immunology and bacterial genetics, we are aiming to identify virulence determinants of F. tularensis and understand critical aspects of the host's immune response to this important human pathogen. His laboratory's recent findings included: identification of novel virulence factors of F. tularensis that restrict macrophage activation through their ability to preserve kinase signaling and proinflammatory cytokine production. Dr. Bakshi's laboratory has made significant progress towards defining the virulence mechanisms and identification of F. tularensis encoded factors, especially the robust antioxidant defense mechanisms responsible for immune subversion caused by F. tularensis. Dr. Bakshi believes that knowledge of Francisella factors that suppress immunity and contribute to pathogenesis may lead to improved therapeutics and effective vaccines against tularemia.
Education
- Ph.D., Indian Veterinary Research Institute
- Postdoct., Institute for Animal Health and Albany Medical College
Research
Dr. Bakshi's laboratory has made significant progress towards defining the virulence mechanisms and identification of F. tularensis encoded factors, especially the robust antioxidant defense mechanisms responsible for immune subversion caused by F. tularensis. My research goals include: understanding how F. tularensis antioxidants subvert macrophage microbicidal activity; and determination of redox-sensitive signaling components that control macrophage signaling and pro-inflammatory cytokine production in response to F. tularensis infection.We have in hand both in vitro and in vivo models that faithfully replicate tularemia and a well equipped Biosafety Level-3 (BSL-3) laboratory to work with the highly virulent SchuS4 strain of F. tularensis.
