Post Doctoral Researcher, Microbial Infection and Immunity
Laboratory of
Dr. Purnima Dubey
750 Biomedical Research Tower (BRT)
460 W 12th Ave, Columbus OH 43210
Phone:
614-293-1045
kyle.caution@osumc.edu
Research Interests
My primary research interest is the characterization of immune pathways activated by pathogenic bacteria. Mechanistic characterization of these host pathways provides a foundation to investigate new treatments and therapies to target medically relevant pathogens. My doctoral work concentrated on elucidating unique, innate immune responses undertaken by alveolar macrophages in response to the respiratory pathogen
Legionella pneumophila. Specifically, identifying novel non-apoptotic functions of caspase-11 and -1 downstream of inflammasome activation resulting in cytoskeletal rearrangement to promote phagolysosomal fusion and the destruction of the intracellular niche. In addition, immediately following my PhD thesis, my postdoctoral work concentrated on elucidating the role of epigenetic regulation of autophagy genes in the cystic fibrosis (CF) lung during
Burkholderia cenocepacia infection. Dysregulation of the autophagic pathway is a central cause of pathology in the CF lung leading to a detrimental cycle of inflammation, infection, and tissue damage. Uncovering a molecular basis for disease progression has helped my work in identifying the green tea component EGCG as a potential therapy to target autophagy gene regulation and promote functional autophagy as a host defense mechanism against lung pathogens. This extensive training has helped develop strong technical and analytical skills that have been extremely useful in studying host-pathogen interactions and the resulting immune responses.
Currently, Dr. Caution’s research activities in Dr. Dubey’s lab focus on developing a more efficacious whooping cough vaccine against
Bordetella pertussis (
B.p.) by investigating Bordetella polysaccharide (Bps) as a potential vaccine candidate. In addition, my research also focuses on characterizing the innate lymphoid cell (ILC) response during challenge in a mouse model. We are interested in how this cell population provides crucial early help to CD4+ T helper cells to promote the clearance of the pathogen. This findings are significant two-fold, as they help us better understand the overall immune response to
B.p., but also could direct vaccine candidates to activate these cells to promote a robust host response.
