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Since the discovery of Helicobacter pylori, the urease activity of this bacterial pathogen has been identified as the key factor in infection and acid acclimation in the human stomach. Ureolytic activity plays a key role in the pathogenesis of several bacteria, and urease has also been described as an emerging pathogenic factor during fungal infection. However, urease produced by the oral bacteria community has been shown to counteract caries, and caries-free subjects have high levels of urease activity in plaque samples. Some lactic acid bacteria with documented probiotic behavior are urease-positive. Likewise, other lactic acid bacterial species that are widely used in yogurt production and other fermented dairy products use urease activity to counteract acid stress and to feed several biosynthetic pathways with carbon dioxide and ammonia derived from urea hydrolysis. Urease is also diffused in several species belonging to the human gut microbiota, and it is estimated that this complex microbial community is able to hydrolyze 15%-30% of the urea synthesized in normal subjects. In this context, urease was proposed to serve as a microbial biomarker to distinguish microbiomes based on age and geography, thus highlighting the crucial involvement of this enzymatic activity in nitrogen recycling when dietary nitrogen is limiting. In light of these considerations, the designation of urease as a microbial virulence factor would be misleading, and the proposed use of urease as a therapeutic target to counteract microbial infections should be carefully evaluated.
Mora et al. (Thu,) studied this question.
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