The focus of our research is to gain a better understanding of how aerosolized pathogens successfully infect and modulate the pulmonary environment to cause overt disease and death. Currently, our principal interest is the pathogenesis of aerosolized F. tularensis, the causative agent of pneumonic tularemia.
There are two primary areas of research ongoing in our laboratory: innate immunity to F. tularensis, and modulation of human cells by F. tularensis. We are particularly interested in modulation of primary antigen-presenting cells (dendritic cells and macrophages) by F. tularensis and how this modulation allows the bacterium to initially evade host immune responses immediately following infection. We utilize both in vivo and in vitro models of disease to reveal specific mechanisms at play in both host and pathogen to gain a better understanding of the dynamic nature of this disease.
Dr. Bosio graduated from Washington State University cum laude with a B.Sc. in 1993. Following completion of her Ph.D. at Colorado State University in 1998, Dr. Bosio completed postdoctoral fellowships at the Food and Drug Administration Center for Biologics Evaluation and Research and at the U.S. Army Medical Research Institute for Infectious Diseases, studying innate immunity to Mycobacterium tuberculosis, F. tularensis, Marburg virus, and Ebola virus. Prior to joining NIAID in 2007, Dr. Bosio was an assistant professor at Colorado State University in the department of microbiology, immunology, and pathology. Dr. Bosio’s laboratory studies the host response to pulmonary pathogens, with special emphasis on virulent F. tularensis and dendritic cells, macrophages, and monocytes.
- Roberts LM, Wehrly TD, Ireland RM, Crane DD, Scott DP, Bosio CM. Temporal Requirement for Pulmonary Resident and Circulating T Cells during Virulent Francisella tularensis Infection. J Immunol. 2018;201(4):1186-1193.
- Schwarz B, Sharma L, Roberts L, Peng X, Bermejo S, Leighton I, Massana AC, Farhadian S, Ko AI, Yale IMPACT Team., Cruz CSD, Bosio CM. Severe SARS-CoV-2 infection in humans is defined by a shift in the serum lipidome resulting in dysregulation of eicosanoid immune mediators. medRxiv. 2020.
- Roberts LM, Evans TJ, Bosio CM. T Cell Metabolism Is Dependent on Anatomical Location within the Lung. Immunohorizons. 2019;3(9):433-439.
- Jessop F, Buntyn R, Schwarz B, Wehrly T, Scott D, Bosio CM. Interferon Gamma Reprograms Host Mitochondrial Metabolism through Inhibition of Complex II To Control Intracellular Bacterial Replication. Infect Immun. 2020;88(2).
- Jessop F, Schwarz B, Heitmann E, Buntyn R, Wehrly T, Bosio CM. Temporal Manipulation of Mitochondrial Function by Virulent Francisella tularensis To Limit Inflammation and Control Cell Death. Infect Immun. 2018;86(8).
Related Scientific Focus Areas
Microbiology and Infectious Diseases
This page was last updated on Saturday, August 14, 2021