Predoctoral Fellow, Year 3
Department of Physiology and Cell Biology
Center of Lung Biology
University of South Alabama College of Medicine
Department of Physician Assistant Studies
University of South Alabama Pat Capps Covey College of Allied Health Professions
PA 514 Introduction to Infectious Disease
PA 520 Clinical Medicine II – Pulmonology
Mentor: Troy Stevens, Ph.D.
Lenoire Locke Professor and Chair, Department of Physiology and Cell Biology
Director, Center for Lung Biology
Focus: My research focuses on host-pathogen interactions in the context of the nosocomial pneumonia that often precedes acute lung injury and ARDS. As Pseudomonas aeruginosa is the prevalent agent of hospital-acquired pneumonia, the type III secretion system effectors ExoU and ExoY are of particular interest to us due to their ability to elicit cytotoxic amyloid prions from the pulmonary endothelium. Amyloid prions are found in the blood, cerebrospinal fluid, and bronchoalveolar lavage fluid of critically ill patients recovering from nosocomial pneumonia. These patients often experience increased rates of end-organ damage, mortality, and neurocognitive decline post-discharge. ExoY, in particular, is present in roughly 90% of clinical strains and we have found that it effectively abolishes the endothelial innate immune response while promoting the release of cytotoxic amyloid prions that are capable of breaching the blood-brain barrier and inducing suppression of learning and memory in animal models.
2017 Grover Conference Young Investigator Award
in recognition of outstanding research related to the pulmonary circulation.
ACTIVE GRANT SUPPORT
NIH T32 Predoctoral Training Grant HL076125, 2016-present
1. Petranka, J, Hopey M, Jennings B, Baird S, and Boone S. 1994. Breeding habitat segregation of wood frogs and American toads: the role of interspecific tadpole predation and adult choice. Copeia 1994:691–697.
2. Lin M, Balczon R, Pittet J-F, Wagner B, Moser S, Morrow K, Voth S, Francis M, Leavesly S, and Stevens T. Nosocomial pneumonia elicits neurotoxic amyloid disease. Nature Medicine, submitted, 2017.
3. Voth S, Francis M, Balczon R, Pittet J-F, Wagner B, Moser S, and Stevens T. Type III secretion system functionality determines the modality of endothelial amyloids following Pseudomonas aeruginosa infection, in preparation, 2017.
1. Voth S, Balczon R, Audia J, and Stevens T. Lung infection elicits endothelial amyloids with distinguishable antimicrobial and cytotoxic properties. The Grover Conference. Sedalia, CO; September 6-10th, 2017.
2. Voth S, Balczon R, Audia J, and Stevens T. Endothelial amyloids: Functional or pathologic? Gordon Conference and Symposium on Biology of Acute Respiratory Infection. Ventura, CA; March 17-23rd, 2018 (Accepted).
3. Voth S, Lin M, Balczon R, Francis M, and Stevens T. Nosocomial lung infection induces a pulmonogenic prionopathy that disrupts the endothelial barrier of the brain. American Thoracic Society Conference. San Diego, CA; May 18-23rd, 2018 (Submitted).
4. Voth S, Balczon R, Francis M, and Stevens T. Pseudomonas aeruginosa Exoenzyme Y intoxication reversibly converts antimicrobial endothelial amyloids into amyloid prions. American Thoracic Society Conference. San Diego, CA; May 18-23rd, 2018 (Submitted).
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