ArticleNature communications2022
Human serum triggers antibiotic tolerance in Staphylococcus aureus.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 92 citations in OpenAlex.
- Biotope-dependent resistance to reactive oxygen species, antibiotic tolerance, and virulence of Staphylococcus aureus.Communications biology · 2026Article
- Orthogonal cell division mediated by PcdA organizes surface virulence factors to drive staphylococcal abscess community formation.Cell reports · 2026Article
- Acquired mutations in transcriptional regulatorAntimicrobial agents and chemotherapy · 2026Article
- Commonly prescribed medicines antagonise anti-MRSA antibiotics and select for resistance.Microbiology (Reading, England) · 2026Article
- Human serum triglycerides promote Staphylococcus aureus biofilm formation and antibiotic tolerance.NPJ biofilms and microbiomes · 2026Article
- Article
- Alanine Uptake Is Required to MaintainMicroorganisms · 2026Article
- Host-driven remodelling of theMicrobiology (Reading, England) · 2026Review
- Unlocking the secret tomSystems · 2026Article
- Polygenic, cell-envelope adaptations drive high-frequency daptomycin resistance inAntimicrobial agents and chemotherapy · 2026Article
- LL-37: Biological Mechanisms and Emerging Therapeutic Applications in Intestinal Disease.Immunity, inflammation and disease · 2026Review
- Integrated multi-omics reveals coordinatedmSystems · 2026Article
- Orthogonal cell division organizes surface virulence factors to drive staphylococcal abscess community formation.bioRxiv : the preprint server for biology · 2026Article
- Expression patterns of core metabolic genes and elevated intracellular ROS confer drug tolerance inMicrobiology spectrum · 2026Article
- Methicillin-resistant and susceptible Staphylococcus aureus: tolerance, immune evasion and treatment.Nature reviews. Microbiology · 2026Review
- The innate immune protein calprotectin ablates the bactericidal activity of β-lactam antibiotics.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Expression ofmBio · 2025Article
- Bergeyella cardium variant induces a unique cytoplasmic vacuolization cell death floatptosis in macrophage.Cell discovery · 2025Article
- Evolution of polyamine resistance inmSphere · 2025Article
- The impact of bacterial purine metabolism on antibiotic efficacy.npj antimicrobials and resistance · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Staphylococcus aureus frequently causes infections that are challenging to treat, leading to high rates of persistent and relapsing infection. Here, to understand how the host environment influences treatment outcomes, we study the impact of human serum on staphylococcal antibiotic susceptibility. We show that serum triggers a high degree of tolerance to the lipopeptide antibiotic daptomycin and several other classes of antibiotic. Serum-induced daptomycin tolerance is due to two independent mechanisms. Firstly, the host defence peptide LL-37 induces tolerance by triggering the staphylococcal GraRS two-component system, leading to increased peptidoglycan accumulation. Secondly, GraRS-independent increases in membrane cardiolipin abundance are required for full tolerance. When both mechanisms are blocked, S. aureus incubated in serum is as susceptible to daptomycin as when grown in laboratory media. Our work demonstrates that host factors can significantly modulate antibiotic susceptibility via diverse mechanisms, and combination therapy may provide a way to mitigate this.
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.