Effect of ammonium on bacterial adherence to bladder transitional epithelium.
The virulence of urease-producing bacteria depends on the ability of urease to degrade urea into ammonia and thereby to alkalinize the urine. Infections caused by urease-producing organisms such as Proteus mirabilis are particularly difficult to manage clinically. We have shown that the layer of glycosaminoglycans at the bladder surface protects against infection by blocking the adherence of bacteria to the epithelium. To determine whether urease-producing urinary pathogens owe their virulence in part to an ability to inactivate the protective effect of the glycosaminoglycan layer, we tested the ability of ammonium chloride to alter bacterial adherence to the normal vesical mucosa. We used an in vivo adherence assay that we have described previously in rabbits. Control animals received sodium chloride adjusted to the same pH as the ammonium chloride. We found that 0.25 M ammonium chloride significantly increases bacterial adherence to normal vesical mucosa as compared to adherence in controls receiving 0.25 M sodium chloride (p less than 0.05). These data suggest that urease plays a hitherto undescribed role in bacterial virulence by altering the antiadherence activity of the glycosaminoglycan layer present at the transitional cell surface.
D000268:Adhesiveness; D000643:Ammonium Chloride / Q000494:pharmacology*; D000818:Animals; D004848:Epithelium / Q000382:microbiology; D004926:Escherichia coli / Q000472:pathogenicity* / Q000502:physiology; D009092:Mucous Membrane / Q000382:microbiology; D011817:Rabbits; D001743:Urinary Bladder / Q000382:microbiology*; D014774:Virulence / Q000187:drug effects
D000643:Ammonium Chloride