The Emerging Role of Urease as a General Microbial Virulence Factor
Figure 1
Model of urease function during fungal infection via the lungs.
Following the inhalation of spores, yeasts germinate in the lungs. If the initial infection is not cleared due to a defective host immune response, yeast cells proliferate. Urea is present in the epithelial lining fluid of the lungs, and the urease-dependent secretion of ammonia from yeast cells further inhibits immune function by impairing phagocyte function and contributes to lung tissue damage. Individual yeast cells gain access to the bloodstream in damaged areas and circulate in the body until becoming trapped in small capillary beds. Circulating urea is then metabolised by the trapped yeast, resulting in ammonia secretion and damage to the epithelial cells of the capillary beds, enabling yeast cells to cross and proliferate in host organs.