Bacterial adhesion
H. pylori mucosal adherence↓
Also searched as H. pylori mucosal adherence.
Adhesion is a non-lethal function, so blocking it applies almost no selective pressure — the published reason anti-adhesives are far less likely to breed resistance than antibiotics. Loosen the grip and normal gastric turnover does the rest.
In depth
Attachment of H. pylori to the gastric epithelium — the adhesin-receptor binding (BabA, SabA, HpaA) that holds the organism against the mucus layer instead of letting it be swept away.
What it drives
It increases H. pylori.
The grip that keeps the organism in place instead of being swept away with the mucus. Verbatim, PMC3307715 (P. freudenreichii JS, single agent): it ‘decreased the adhesion of Helicobacter pylori to Caco-2 intestinal cells when used individually’. independent group, PMID 30806251 (Hericium erinaceus): it ‘inhibited H. pylori adhesion capacity to human gastric epithelial cell line (AGS), even when added at a concentration that affected neither H. pylori nor AGS viability’ — adhesion blockade independent of killing. Third stream, J Ethnopharmacol 2024 S0378874124006950 (Phellodendron chinense, immunofluorescence adhesion assay). Why it is a colonization lever and not an eradication claim, in the literature’s own words: these agents are ‘less likely to generate resistance... since adhesion is a nonlethal function’. PMID 30806251 · PMC3307715
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.