![]() These findings suggest that the galU gene is required for corneal infection and for efficient systemic spread following lung infection but is not required for infection confined to the lung. In an acute pneumonia model, the 50% lethal doses of the galU mutants were higher than those of the corresponding wild-type strains, yet these mutants could cause mortality and severe pneumonia, as judged by histology, even with minimal systemic spread. In a corneal infection model, the galU mutants were significantly attenuated. The galU mutants were more serum sensitive than the parental strains but remained cytotoxic in vitro. We studied galU mutants of strain PAO1, of its cytotoxic variant expressing ExoU from a plasmid, and of the inherently cytotoxic strain PA103. ![]() Here we evaluated the role of the galU gene in the pathogenesis of murine lung and eye infections and in cytotoxicity due to the TTSS effector ExoU. aeruginosa results in production of a rough LPS and truncated LPS core. ![]() We previously reported that interruption of the galU gene in P. It is not clear whether an LPS-rough phenotype affects cytotoxicity related to the type III secretion system (TTSS). aeruginosa, which lack O antigen, can survive in the lung and cause chronic infection. In cystic fibrosis patients, however, LPS-rough strains of P. Turns out they don’t qualify as support animals.Acute pneumonias and corneal infections due to Pseudomonas aeruginosa are typically caused by lipopolysaccharide (LPS)-smooth strains. Once after a visit back home, I was stopped by TSA agents for trying to carry two live lobsters on a plane. I grew up on the coast of New York and I love fresh seafood. I enjoy reading, running (Atlanta’s hills are no joke), being with our dogs (we have three rescues), and renovating our 100-year-old home. What do you like to do in your spare time? This is easy one - Emory has a friendly, inclusive, and collaborative culture that I love. We are particularly interested in the metabolic programs that govern neutrophilic lung inflammation and the bacterial molecules that drive neutrophil activation and recruitment to the lung. Our research focuses on both host and pathogen factors that modulate neutrophilic lung inflammation during bacterial pneumonia. The host inflammatory response to pneumonia must be balanced with sufficient inflammation to control the bacterial infection without the excessive inflammation that can cause tissue damage. Why is it important?īacterial pneumonia is a common and severe lung infection that is a leading cause of death worldwide. ![]() I work in the Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, and I am very fortunate to have David Guidot as a mentor.īriefly describe your research. In what division do you work, and who is your mentor? I have a research program focused on neutrophilic inflammation during bacterial pneumonia. I recently moved from Vanderbilt to Emory University in July 2021 and currently serve as the acting medical director of the EUH 4a/6a ICU. I received an MD/PhD from Virginia Commonwealth University and completed postgraduate training in internal medicine, infectious diseases, and pulmonary and critical care medicine at Vanderbilt University, where I joined the faculty in 2016. I am a pulmonary and critical care medicine physician-scientist.
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