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Treatments for urologic infections may change host environment
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Several abstracts from this year's AUA annual meeting suggest that, just as bacteria alter their host environment to their benefit, treatments for infection and inflammation may counter by changing the host environment to pathogens' detriment.
Key Points
Several abstracts from this year's AUA annual meeting suggest that, just as bacteria alter their host environment to their benefit, treatments for infection and inflammation may counter by changing the host environment to pathogens' detriment.
"We used to think that these were predominantly reinfections by bacteria entering the urinary tract from the outside-in," said Dr. Schaeffer. "But these papers begin to support the concept of relapse from within due to modulation of host defenses. Emerging evidence shows that some bacteria are able to establish a pod or colony within the surface or deeper transitional epithelium, where they can reside until they re-emerge and cause a recurring infection from within the urinary tract."
"B1 cells in turn suppress the neutrophil influx, decreasing bacterial clearance. Here, the bacterium is skewing the Th2 cytokine response to provide an environment that allows it to persist within the urinary tract. This is one of the prerequisites for establishing an intercellular pod," Dr. Schaeffer said.
Another abstract may explain through an animal model why diabetic patients have difficulty resisting and clearing bladder infections, said Dr. Schaeffer.
"These researchers showed that delayed clearance in diabetic mice occurred due to a lower, postponed expression of other cytokines-macrophage inflammatory protein-2 and monocyte chemotactic protein-1-which are normally proactive in clearing the urinary tract of pathogens," he said. Due to low levels of these cytokines, investigators concluded, diabetic mice experienced impaired neutrophil recruitment and therefore took much longer than controls to clear induced cystitis.
Subsequently, the guanosine triphosphate hydrolase (GTPase) Rab27b allows uropathogenic Escherichia coli to gain access to urothelial cells because it mediates adherence, invasion, and trafficking within these cells, according to a third abstract he highlighted.
"These investigators postulate that this process is also modified by genetic factors. Individuals who are more susceptible to infections may have increased expression of this molecule, which accentuates a pathogenic invasion," he said.
