BACKGROUND
Urinary tract infections (UTIs) are one of the most frequent bacterial infections affecting both male and female populations. However, women are more susceptible to UTIs 50%-60% acquire one in their lifetime. 25% of women acquire recurrent UTIs shortly after the first infection, which can lead to kidney failure. Pregnant or postmenopausal women are more prone to experience these, indicating the hormonal etiology of UTI pathogenesis. Recently, the Food and Drug Administration (FDA) has approved the use of vaginal estrogen suppositories for postmenopausal UTI patients, but these are not effective in all women and the underlying immunomodulatory mechanics of action of estrogen in the urinary tract remain poorly understood. Therefore, it is important to understand the underlying molecular pathways by which estrogen modulates UTI pathogenesis that result in differential innate immune responses in the bladder and kidney.
SUMMARY OF TECHNOLOGY
Researchers at OSU have developed a method for boosting innate immune responses to fight UTIs. Estrogen receptor-based agonists and GPR30 antagonists to are used to boost or modulate the activity of complement regulatory proteins or their receptors since there are differential effects of these receptor analogs on the epithelial cell innate immune responses during homeostasis, thus the epithelial cells can assist in clearing the recurrent urinary tract infections in high-risk individuals. This method has been demonstrated with bladder and kidney cell lines, and differ with homeostasis versus pathogenesis, affecting infection outcome. The estrogen receptor-based novel approach provides the advantage of not only treatment of UTIs but can act as a prophylactic to prevent them from occurring. Additionally, this can treat multi-drug resistant uropathogens, which are a growing concern.
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STAGE OF DEVELOPMENT
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