ArticleBMC microbiology2026
Beyond antibiotics: a new anti-virulence strategy combating ESBL-producing Klebsiella pneumoniae by targeting periplasmic trehalase.
Article in BMC microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe rise of ESBL-producing Klebsiella pneumoniae (ESBL-Kp) poses a serious public health threat with high mortality and limited treatment options due to its broad resistance. This study investigates the role of the periplasmic trehalase (TreA) which is associated with virulence and significantly upregulated in resistant strains, to identify potential new therapeutic strategies.
methodsWe generated a treA-deficient mutant (ΔtreA) from an ESBL-Kp isolate and conducted a phenotypic comparison with the wild-type strain. The assessments focused on their growth, tolerance to temperature stress, survival in antibiotic-treated macrophages, biofilm formation, and virulence in a murine lung infection model.
resultsDeletion of treA significantly impaired bacterial growth and reduced biomass during the stationary phase. The mutant displayed compromised thermotolerance at elevated temperatures. Under antibiotic treatment, ΔtreA exhibited reduced intracellular survival in macrophages and diminished proliferative capacity after antibiotic adaptation. Biofilm formation was significantly attenuated, with lower optical density values observed across all dilutions. In murine models, treA deficiency led to reduced virulence, as evidenced by improved survival rates, less weight loss, and lower pulmonary bacterial loads.
conclusionTreA acts as a key metabolic determinant for virulence in ESBL-Kp, underscoring its potential as a target for anti-virulence strategies against this multidrug-resistant pathogen.
Indexed as
Identifiers
What Socratic 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 Socratic graph.