Urea protects Helicobacter (Campylobacter) pylori from the bactericidal effect of acid.
Level 5 - mechanism / opinion, no new human data
In vitro bench experiment without human subjects
PubMed 2379775 · doi:10.1016/0016-5085(90)90957-3
What was done
Authors tested the pH susceptibility of Helicobacter pylori, Proteus mirabilis, and urease-negative Campylobacter jejuni in vitro in the presence and absence of urea to determine whether urease-mediated ammonia generation protects H. pylori from gastric acid.
What was found
Without urea, all three bacteria were highly susceptible to acid. The addition of 5 mmol/L urea completely protected H. pylori from pH levels as low as 1.5, while P. mirabilis and C. jejuni were not protected. Urea protected H. pylori at concentrations down to 0.05 mmol/L. Specific quantitative survival counts and variance values were not reported in the abstract.
Why it matters
It demonstrates a direct mechanism by which H. pylori exploits urea and high urease activity to survive bactericidal gastric acid.
Limits
This is an in vitro bench study without human or animal subjects, lacking in vivo physiological complexity such as gastric mucosal barriers. The abstract does not report sample sizes, replicate counts, or precise quantitative bacterial survival rates.
Cited by
- supports Helicobacter pylori utilizes the urease enzyme to neutralize stomach acid and create a microenvironment of neutral pH in the gastric mucosa.