Postdoctoral Research: The current research focus of our work is in the area of Host-Pathogen Interaction and Molecular Infection Biology. In our recent work to unravel cellular and molecular mechanism of Listeria pathogenesis, we have shown Listeria uses Listeria adhesion protein (LAP) as a weapon to cross intestinal epithelial barrier. We reported LAP facilitates adhesion of Listeria by interacting with host Hsp60 receptors on intestinal epithelial cells in mouse model as well as in human colon cancer cell line (Caco-2). LAP-Hsp60 interaction activates NFκB signaling to redistribute epithelial junctional proteins (claudin-1, occluding and E-cadherin) by activating MLCK. This, in turn, opens epithelial barrier to facilitate translocation of L. monocytogenes through gut barrier (Drolia et al., 2018. Cell Host & Microbe). L. monocytogenes causes gastroenteritis in healthy individuals but bacterial factors that contribute to gastroenteritis are not known. In our latest study, we found LAP as a major player to mediate gastroenteritis in mouse model (under preparation-2019).
On the other hand, we are using probiotics approach to understand and control enteric pathogens interactions in the gut of the host. By using a Next-Generation Probiotic Strain (NGPS) we are investigating the potential of NGPS to prevent colonization and infection of enteric pathogens including Listeria and enterotoxigenic Escherichia coli in mouse model. In our current studies, we got promising outcomes as NGPS could prevent epithelial barrier dysfunction and dissemination of L. monocytogenes in intestinal and extra intestinal organs of mice upon NGPS exposure (under preparation-2019). Also, we plan to test these findings in swine model.
Doctoral Research: My Doctoral research was focused on a Ser/Thr and Tyr kinase from Helicobacter pylori. We demonstrated, for the first time, that JHP040 (CtkA), a putative virulence factor, is secreted by H. pylori and exposed to the immune system of the human host. This bacterial factor acts as an autophosphorylating tyrosine kinase and induces apoptosis in mouse macrophages (Tenguria et al., 2014. Int J Med Microbiol). In another study, we were able to show that TieA (HP0986), another virulence factor from H. pylori acts as TNFR1 interacting endonucleaseA (Devi et al., 2016. Nucleic Acid Research). It interacts with cultured gastric epithelial cells and localizes in cytosol and nucleus, and induces IL-8 secretion via NFκB pathway (Devi et al., 2014. Helicobacter). Furthermore, we found that TieA activates apoptotic-signaling pathway by interacting with TNFR1 in cultured macrophages (Ansari et al., 2014. Cytokine).