The Helicobacter pylori UreI protein: role in adaptation to acidity and identification of residues essential for its activity and for acid activation.
Level 5 - mechanism / opinion, no new human data
Bench in vitro bacterial molecular genetics and biochemical assays
PubMed 11737644 · doi:10.1046/j.1365-2958.2001.02689.x
What was done
Researchers investigated the functional role and critical amino acid residues of the inner membrane protein UreI directly in *Helicobacter pylori*. They measured extracellular ammonia production in wild-type strains exposed to acidic conditions (pH ≤ 5) in the presence of urea or acetamide. To identify residues essential for low-pH activation and transport function, they generated *H. pylori* chromosomal mutant strains targeting four conserved histidine residues (H71, H123, H131, H193) and four residues within the third intracellular loop (L165, G166, K167, F168).
What was found
Wild-type *H. pylori* displayed rapid stimulation of extracellular ammonia production upon exposure to pH ≤ 5 in the presence of urea, but no stimulation occurred when acetamide was substituted. Mutational analysis revealed that mutating residue H193 (unlike H123 identified in prior heterologous oocyte models) abolished low-pH stimulation and uncoupled UreI activity from acid activation. Mutations across the third intracellular loop (L165, G166, K167, F168) impaired baseline UreI activity. Quantitative kinetic values and sample sizes were not reported in the abstract.
Why it matters
This study defines the native molecular gating mechanism of UreI in *H. pylori*, pinpointing His-193 as the key residue required for acid activation of urea transport, a critical pathway for bacterial acid survival in the stomach.
Limits
The abstract reports no quantitative values, effect sizes, statistical bounds, or replicate numbers. As an in vitro microbiological study, direct translation to in vivo clinical infection dynamics is not evaluated in the abstract.
Cited by
- supports Helicobacter pylori survives in the stomach by secreting alkaline ammonia to neutralize stomach acid.