|Pathogenic bacteria are confronted by a number of host innate immune responses that are intended to kill the invading organisms. The production of oxidative radicals is a primary function of the innate cells. We have demonstrated that the ability to repair DNA damage incurred by oxidative stress is essential for the virulence of uropathogenic Escherichia coli. We hypothesize that other stress responses will be critical for the survival of Escherichia coli in the host. We are currently determining the stress responses induced in the presence of activated innate immune cells.|
|Approximately 25% of the preterm births in the U.S are due to maternal urinary tract infection. Although there is a strong link between maternal urinary tract infection and preterm birth, nothing is known regarding how infection within one organ can affect the status of another isolated organ. We have successfully developed a mouse model for urinary tract infection-mediated preterm birth. Similar to that seen in the human population, infected mice deliver early with low birth weight pups with reduced viability. We are currently investigating the immunological effectors induced against urinary tract infection that are transmitted to the uterus to induce preterm delivery|
|Renal scaring is the leading cause of renal failure and results from inflammation within the kidney due to pediatric urinary tract infections. It is unclear why some children are susceptible to renal scaring even in the absence of Pyelonephritis (kidney infection). We hypothesize that bacterial strains that cause pediatric urinary tract infections will induce a strong immune response that results in inflammation of the kidney and renal scars. We are currently investigating the pathogenic phenotypes of a number of pediatric uropathogens to identify potential bacterial factors that are associated with renal scaring.|
Inhibition of cell division in the presence of continued bacterial growth results in the formation of a filamentous morphology. A number of pathogens appear to change their morphology into filamentous forms in models for disease. We have demonstrated that the filamentous form protects uropathogenic Escherichia coli from killing by phagocytes. We are also determining the bacterial and host factors that are responsible for morphological changes that lead to protection from phagocyte killing.
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