ArticleMicrobial biotechnology2026
Betulinic Acid Eradicates Implant-Associated Infections by Disrupting the S. aureus Biofilm Matrix and Potentiating Host Immune Clearance.
Article in Microbial biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Repurposing trifluridine as an anti-Staphylococcus aureus agent targeting virulence factor staphyloxanthin and attachment genes.Scientific reports · 2026Article
- Betulinic Acid Eradicates Implant-Associated Infections by Disrupting the S. aureus Biofilm Matrix and Potentiating Host Immune Clearance.Microbial biotechnology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Staphylococcus aureus biofilms are major contributors to chronic and recurrent infections due to their intrinsic tolerance to antibiotics and host immune clearance, highlighting the urgent need for safe and effective antibiofilm strategies. This study evaluated the inhibitory effects and underlying mechanisms of betulinic acid (BA), the principal active constituent of the traditional Chinese medicine Liquidambaris fructus, against S. aureus biofilms. In vitro assays demonstrated that the minimum biofilm inhibitory concentration (MBIC) of BA was 32 μg/mL, which was markedly lower than its minimum inhibitory concentration (MIC, 512 μg/mL), indicating preferential activity against biofilm formation. Serial passage experiments revealed no detectable induction of drug resistance. Mechanistic studies revealed that BA suppressed early biofilm adhesion and aggregation, downregulated the expression of adhesion-related genes (clfA, clfB, fnbpA and fnbpB), and reduced the production of extracellular polysaccharide (EPS) and extracellular DNA (eDNA). BA further disrupted mature biofilm architecture, promoted macrophage infiltration, enhanced bacterial clearance and attenuated the expression of immune evasion factors (scin, chip, lukE and nuc). In vivo, BA significantly alleviated implant-associated infections, mitigated local inflammatory responses and facilitated tissue repair. Collectively, these findings reveal that BA inhibits S. aureus biofilms through multiple coordinated mechanisms, with a low propensity for resistance development and favourable biosafety, supporting its potential as a promising lead compound for the development of novel antibiofilm therapeutics.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.