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Oxidative stress is not always a bad thing. In fact, the generation of high levels of reactive oxygen and chlorine species (RO/CS) plays an important physiological role in the innate immune response. Production of RO/CS, including hypochlorous acid (HOCl), provides a powerful strategy for killing invading pathogens including Gram-negative uropathogenic E. coli (UPEC) and Pseudomonas aeruginosa. UPEC are the culprits of the vast majority of urinary tract infections (UTIs) and differ significantly from intestinal E. coli by their ability to survive and persist in the urinary tract. The opportunistic pathogen P. aeruginosa is responsible for many of the known infections that affect patients with UTIs, cystic fibrosis, and acute traumatic burns. Hallmarks of these diseases include sustained inflammation, excessive neutrophil infiltration, and the uncontrolled production of high levels of HOCl by myeloperoxidases. HOCl is extremely reactive and bactericidal, even at low micromolar concentrations, damaging many cellular components including proteins, DNA, lipids, and cofactors. However, very little is known about how inflammation-associated pathogens sense and defend RO/CS. The bacterial response and defense strategies are expected to be critical for their ability to survive immune cell attacks and therefore likely impact the disease progression. Hence, our long-term goal is to understand the RO/CS stress responses in medically relevant bacteria and to define the role of these defense strategies during colonization and pathogenesis.

  1. How do uropathogenic E. coli respond to and defend reactive oxygen and chlorine species?
  2. How do Pseudomonas aeruginosa respond to and defend reactive oxygen and chlorine species?
  3. What is the role of inorganic polyphosphate in Pseudomonas aeruginosa-mediated killing of Staphylococcus aureus?
  4. Investigating the killing mechanism of novel antimicrobial agents

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