Thomas Scot Murray MD, PhD

Assistant Professor (Adjunct) of and Assistant Professor of Laboratory Medicine

Research Interests

Pseudomonas aeruginosa motility and pathogenesis; Detection of drug resistant gram negative bacterium

Current Projects

Mechanisms of Pseudomonas aeruginosa pulmonary colonization

The role of lactate metabolism in P.aeruginosa pulmonary infection

Studies to determine the most sensitive method to screen for carbapenemase producing Klebsiella (KPC)

Research Summary

Children with the genetic disease Cystic Fibrosis get multiple lung infections with a bacteria called Pseudomonas aeruginosa. These infections lead to frequent hospitalizations and a decreased quality of life for these children. Pseudomonas infections are difficult to treat because the bacteria form organized communities called biofilms that are often resistant to antibiotics. Dr Murray’s research focuses on understanding how Pseudomonas causes infection and forms biofilms in the lungs of children with cystic fibrosis. Dr Murray’s recent work has focused on a number of bacterial characteristics that are important for stablishing infection in the lung. He is currently studying how bacteria with different virulence properties interact with mammalian cells to cause damage. The long term goal of this work is to identify new bacterial targets for drug development to help treat and prevent these lung infections.

Extensive Research Description

Dr. Murray’s project, The regulation of surface colonization by Psedomonas aeruginos, uses his preliminary evidencethat certain regulatory proteins produced by P. aeruginosa each controls multiple factors important for colonization. In patients with cystic fibrosis (CF), chronic colonization of the lungs with Pseudomonas aeruginosa results in frequent hospitalizations and in premature mortality. The goals of the project are to determine the components required for surface colonization co-regulated by these proteins, to quantitate the colonization of surfaces by these strains in a CF tissue culture model of infection, and to correlate in vitro surface colonization defects with abnormal chronic colonization in vivo.

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