ArticleCell reports2020
Modulating Isoprenoid Biosynthesis Increases Lipooligosaccharides and Restores Acinetobacter baumannii Resistance to Host and Antibiotic Stress.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Outer membrane remodeling via lipid-peptidoglycan crosstalk enables lipooligosaccharide-deficient colistin resistance.Cell reports · 2026Article
- Prolonged exposure to teixobactin generates cross-tolerance to other cell wall-targeting antimicrobials inAntimicrobial agents and chemotherapy · 2025Article
- Article
- Amino acid competition shapes Acinetobacter baumannii gut carriage.Cell host & microbe · 2025Article
- The interplay betweenInfection and immunity · 2025Article
- The intricacies ofFrontiers in microbiology · 2025Review
- Dietary zinc deficiency promotes Acinetobacter baumannii lung infection via IL-13 in mice.Nature microbiology · 2024Article
- Diclofenac sensitizes multi-drug resistant Acinetobacter baumannii to colistin.PLoS pathogens · 2024Article
- Maintenance of bacterial outer membrane lipid asymmetry: insight into MlaA.BMC microbiology · 2024Review
- Lung Epithelium Releases Growth Differentiation Factor 15 in Response to Pathogen-mediated Injury.American journal of respiratory cell and molecular biology · 2024Article
- Genetic synergy betweenmBio · 2024Article
- The metabolic slowdown caused by the deletion ofAntimicrobial agents and chemotherapy · 2024Article
- Article
- Acinetobacter Metabolism in Infection and Antimicrobial Resistance.Infection and immunity · 2023Review
- Penicillin Binding Protein 7/8 Is a Potential Drug Target in Carbapenem-Resistant Acinetobacter baumannii.Antimicrobial agents and chemotherapy · 2023Article
- Mobile genetic elements in Acinetobacter antibiotic-resistance acquisition and dissemination.Annals of the New York Academy of Sciences · 2022Review
- Assessing the Role of Cold-Shock Protein C: a Novel Regulator of Acinetobacter baumannii Biofilm Formation and Virulence.Infection and immunity · 2022Article
- Gram-negative bacteria act as a reservoir for aminoglycoside antibiotics that interact with host factors to enhance bacterial killing in a mouse model of pneumonia.FEMS microbes · 2022Article
- Identification of Two Variants of Acinetobacter baumannii Strain ATCC 17978 with Distinct Genotypes and Phenotypes.Infection and immunity · 2021Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Acinetobacter baumannii is a leading cause of ventilator-associated pneumonia and a critical threat due to multidrug resistance. The A. baumannii outer membrane is an asymmetric lipid bilayer composed of inner leaflet glycerophospholipids and outer leaflet lipooligosaccharides. Deleting mlaF of the maintenance of lipid asymmetry (Mla) system causes A. baumannii to become more susceptible to pulmonary surfactants and antibiotics and decreases bacterial survival in the lungs of mice. Spontaneous suppressor mutants isolated from infected mice contain an ISAba11 insertion upstream of the ispB initiation codon, an essential isoprenoid biosynthesis gene. The insertion restores antimicrobial resistance and virulence to ΔmlaF. The suppressor strain increases lipooligosaccharides, suggesting that the mechanism involves balancing the glycerophospholipids/lipooligosaccharides ratio on the bacterial surface. An identical insertion exists in an extensively drug-resistant A. baumannii isolate, demonstrating its clinical relevance. These data show that the stresses bacteria encounter during infection select for genomic rearrangements that increase resistance to antimicrobials.
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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.