Immunity to Pulmonary Pathogens Section
Established in 2007
Catharine (Katy) Bosio, Ph.D. (She/Her/Hers)
Chief, Immunity to Pulmonary Pathogens Section
- Innate and adaptive immune responses in the lung
- Immunity to Francisella tularensis, Bordetella pertussis, SARS-CoV-2
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, B. pertussis and SARS-CoV-2 and how these pathogens influence host metabolic responses.
There are two primary areas of research ongoing in our laboratory: innate and adaptive pulmonary immune responses and modulation of human cells by a variety of pathogens of clinical concern. We are particularly interested in modulation of primary antigen-presenting cells (dendritic cells and macrophages) by both bacterial and viral pathogens and how this modulation allows microorganisms to initially evade host immune responses immediately following infection. We utilize both in vivo and in vitro models of disease to reveal the specific metabolic pathways mechanisms modulated in both host and pathogen to gain a better understanding of the dynamic nature of pulmonary disease.
Ph.D., 1998, Colorado State UniversityB.Sc., 1993, Washington State University
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, monocytes, and how metabolic flux plays a role in lung diseases.
Roberts LM, Schwarz B, Speranza E, Leighton I, Wehrly T, Germain R, Best S, and Bosio CM. Pulmonary Infection Induces Scarred Lipidome Influencing Trained Immunity. 2021. iScience. 24:1.
Schwarz B, Sharma L, Roberts L, Peng X, Bermejo S, Leighton I, Casanovas-Massana A, Minasyan M, Farhadian S, Ko AI; Yale IMPACT Team, Dela Cruz CS, Bosio CM. Cutting Edge: Severe SARS-CoV-2 Infection in Humans Is Defined by a Shift in the Serum Lipidome, Resulting in Dysregulation of Eicosanoid Immune Mediators. J Immunol. 2021 Jan 15;206(2):329-334.
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 Aug 15;201(4):1186-1193. PMC6086594.
Ireland R, Schwarz B, Nardone G, Wehrly TD, Broeckling CD, Chiramel AI, Best SM, Bosio CM. Unique Francisella Phosphatidylethanolamine Acts as a Potent Anti-Inflammatory Lipid. J Innate Immun. 2018;10(4):291-305.
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 Jul 23;86(8):e00044-18.
Wyatt EV, Diaz K, Griffin AJ, Rasmussen JA, Crane DD, Jones BD, Bosio CM. Metabolic Reprogramming of Host Cells by Virulent Francisella tularensis for Optimal Replication and Modulation of Inflammation. J Immunol. 2016 May 15;196(10):4227-36.
IPPS studies how virulent pulmonary pathogens, including F. tularensis, B. pertussis, & SARS-CoV-2, evade and inhibit protective immunity in the lung. Our goal is to use this information to devleop novel therapeutics and vaccines against a variety of infectious diseases. We also aim to understand regulation of innate and adaptive immune responses in the lungs with a special emphasis on metabolism.